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1
Escribano, Luis, Alberto Orfao, Jesús Villarrubia, Beatriz Díaz-Agustín, Carlos Cerveró, Agustín Rios, José L. Velasco, Juana Ciudad, José L. Navarro, and Jesús F. San Miguel. "Immunophenotypic Characterization of Human Bone Marrow Mast Cells. A Flow Cytometric Study of Normal and Pathological Bone Marrow Samples." Analytical Cellular Pathology 16, no. 3 (1998): 151–59. http://dx.doi.org/10.1155/1998/341340.
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The goal of the present paper was to define the immunophenotype of bone marrow mast cells (BMMC) from healthy controls and patients with hematologic malignancies (HM) based on the use of multiple stainings with monoclonal antibodies analyzed by flow cytometry. Our results show that BMMC from both groups of individuals display a similar but heterogenous immunophenotype. The overall numbers of BMMC are higher in the HM group of individuals (p= 0.08). Three patterns of antigen expression were detected: (1) markers constantly positive in all cases analyzed (CD9, CD29, CD33, CD43, CD44, CD49d, CD49e, CD51, CD71, CD117, and FcεRI), (2) antigens that were constantly negative (CD1a, CD2, CD3, CD5, CD6, CD11a, CD14, CD15, CD16, CD19, CD20, CD21, CD23, CD25, CD30, CD34, CD38, CD41a, CD42b, CD65, CD66b, HLA-DR, and CD138), and (3) markers that were positive in a variable proportion of cases – CD11b (50%), CD11c (77%), CD13 (40%), CD18 (20%), CD22 (68%), CD35 (27%), CD40 (67%), CD54 (88%) and CD61 (40%). In addition, BMMC from all cases explored were CD45+, and this antigen was expressed at an intensity similar to that of mature granulocytes.In summary, our results show that BMMC from both healthy controls and HM patients display a relatively heterogenous immunophenotype. Interestingly, we have observed clear differences between the immunophenotype of BMMC and MC from other tissues. This could be due either to the heterogeneity of human MC according to their tissue localization or to the sensitivity of the method used for antigen detection.
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Lones, Mark, and Ivan Kirov. "Cell Surface Targets for Monoclonal Antibody Therapy in Lymphoid Neoplasms of Children and Adolescents." Blood 104, no. 11 (November 16, 2004): 4544. http://dx.doi.org/10.1182/blood.v104.11.4544.4544.
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Abstract Recently, monoclonal antibodies have become available for treatment of lymphoid neoplasms in adults, but have not been studied in children and adolescents. These monoclonal antibodies are directed against cell surface antigens CD20 (Rituximab, Ibritumomab-Tiuxetan, Tositumomab), CD22 (Epratuzumab), CD52 (CAMPATH-1H), HLA-DR Beta-chain (Hu1D10), CD23 (IDEC-152), and CD33 (Gemtuzumab Ozogamicin). The objective of this study is to identify cell surface targets eligible for monoclonal antibody therapy in lymphoid neoplasms of children and adolescents. This is a retrospective analysis of lymphoid neoplasms evaluated by flow cytometry immunophenotyping at a single institution from January 2002 to July 2004. All patients were less than 21 years old at primary diagnosis. Flow cytometry immunophenotyping employed a 3-color method. Fluorochrome-conjugated monoclonal antibodies were utilized to detect cell surface antigens: CD20, CD22, CD23 (Becton-Dickinson), and CD52 (CALTAG) conjugated with PE; HLA-DR and CD33 (Becton-Dickinson) conjugated with FITC. For this study, a cell surface antigen was interpreted as positive when neoplastic cells exhibited moderate or bright intensity staining, or interpreted as negative when staining was dim or absent. A total of 95 patients are included in this study. Demographic data: Age <1 to 20 years (median 7); Male=52, Female=43. Diagnoses included: Precursor-B Acute Lymphoblastic Leukemia (Pre-B ALL) = 80, Precursor-T Acute Lymphoblastic Leukemia or Precursor-T Lymphoblastic Lymphoma (Pre-T ALL/LBL) = 11, Burkitt Lymphoma = 4. Total specimens = 105 (primary diagnosis = 82, relapse = 23). Immunophenotyping results for the number of specimens tested are in the Table. Table 1 Diagnosis CD20 CD22 CD52 HLA-DR CD23 CD33 Pre-B ALL 32/86 (37%) 90/90 (100%) 53/57 (93%) 87/87 (100%) 0/15 (0%) 4/90 (4%) Pre-T ALL/LBL 0/11 (0%) 0/11 (0%) 9/10 (90%) 2/11 (18%) 0/5 (0%) 0/11 (0%) Burkitt Lymphoma 4/4 (100%) 4/4 (100%) 3/3 (100%) 3/3 (100%) 0/2 (0%) 0/3 (0%) CD22 was positive (usually bright intensity) in all Pre-B ALL and Burkitt Lymphoma specimens. CD20 was positive in all Burkitt Lymphoma (bright intensity) and in a subset of Pre-B ALL (usually moderate intensity) specimens. CD22 and CD20 were negative in Pre-T ALL/LBL specimens. In a subset, CD52 was positive (moderate to bright intensity) in nearly all specimens. HLA-DR was positive (moderate to bright intensity) in all Pre-B ALL and Burkitt Lymphoma specimens. In a subset, CD23 was negative in all specimens. Also, CD33 was negative in nearly all specimens. In conclusion, lymphoid neoplasms in children and adolescents have cell surface antigens that are eligible targets for currently available monoclonal antibody therapy. Patients with Pre-B ALL are candidates for therapy directed to CD22, CD52, HLA-DR, and a subset to CD20, but not to CD23 or CD33. Patients with Burkitt Lymphoma are eligible for therapy to CD20, CD22, CD52, and HLA-DR, but not CD23 or CD33. Patients with Pre-T ALL/LBL are eligible for therapy to CD52, but not CD20, CD22, HLA-DR, CD23 or CD33. These results indicate that future clinical therapeutic trials can be designed for children and adolescents with lymphoid neoplasms to evaluate monoclonal antibody therapy directed to CD20, CD22, CD52, or HLA-DR, employing single or multiple antibodies as a new modality, in addition to chemotherapy.
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Geisler, CH, JK Larsen, NE Hansen, MM Hansen, BE Christensen, B. Lund, H. Nielsen, T. Plesner, K. Thorling, and E. Andersen. "Prognostic importance of flow cytometric immunophenotyping of 540 consecutive patients with B-cell chronic lymphocytic leukemia." Blood 78, no. 7 (October 1, 1991): 1795–802. http://dx.doi.org/10.1182/blood.v78.7.1795.1795.
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Abstract Blood mononuclear cells from 540 newly diagnosed, unselected patients with B-cell chronic lymphocytic leukemia (CLL) were examined by immunofluorescence flow cytometry for a panel of surface membrane markers, including IgM and IgD, the monoclonal antibodies anti-CD3, -5, -20, -21, -22, -FMC7, and, for the final 125 patients, anti-CD23. There were 503 CD5+ and 37 CD5- cases. In the CD5+ cases, the cells typically expressed IgM, IgD, CD20, CD21, CD22, and CD23. In univariate analysis, age, clinical stage, IgM-fluorescence intensity, CD23, and FMC7 had significant prognostic importance, with high IgM-fluorescence intensity, high FMC7, and low CD23 expression being associated with a short survival. There was no significant difference in survival between 351 cases expressing IgMD and 55 cases expressing IgM without IgD, or between kappa and lambda light chain monoclonal cases. CD20, CD21, and CD22 had no prognostic importance. In Cox multiple regression analyses, age, CD23, IgM-fluorescence intensity, and clinical stage (International Workshop System) had independent prognostic importance. Thus, besides clinical variables, CD23 and IgM intensity might be useful prognostic markers in the management of CD5+, B-cell CLL. The survival of CD5- patients was on the borderline of being significantly shorter than that of CD5+ patients. The majority of the CD5- cases were FMC7+, CD23-, had strong IgM fluorescence, and had splenomegaly.
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Geisler, CH, JK Larsen, NE Hansen, MM Hansen, BE Christensen, B. Lund, H. Nielsen, T. Plesner, K. Thorling, and E. Andersen. "Prognostic importance of flow cytometric immunophenotyping of 540 consecutive patients with B-cell chronic lymphocytic leukemia." Blood 78, no. 7 (October 1, 1991): 1795–802. http://dx.doi.org/10.1182/blood.v78.7.1795.bloodjournal7871795.
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Blood mononuclear cells from 540 newly diagnosed, unselected patients with B-cell chronic lymphocytic leukemia (CLL) were examined by immunofluorescence flow cytometry for a panel of surface membrane markers, including IgM and IgD, the monoclonal antibodies anti-CD3, -5, -20, -21, -22, -FMC7, and, for the final 125 patients, anti-CD23. There were 503 CD5+ and 37 CD5- cases. In the CD5+ cases, the cells typically expressed IgM, IgD, CD20, CD21, CD22, and CD23. In univariate analysis, age, clinical stage, IgM-fluorescence intensity, CD23, and FMC7 had significant prognostic importance, with high IgM-fluorescence intensity, high FMC7, and low CD23 expression being associated with a short survival. There was no significant difference in survival between 351 cases expressing IgMD and 55 cases expressing IgM without IgD, or between kappa and lambda light chain monoclonal cases. CD20, CD21, and CD22 had no prognostic importance. In Cox multiple regression analyses, age, CD23, IgM-fluorescence intensity, and clinical stage (International Workshop System) had independent prognostic importance. Thus, besides clinical variables, CD23 and IgM intensity might be useful prognostic markers in the management of CD5+, B-cell CLL. The survival of CD5- patients was on the borderline of being significantly shorter than that of CD5+ patients. The majority of the CD5- cases were FMC7+, CD23-, had strong IgM fluorescence, and had splenomegaly.
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Polishchuk, Alyona, Michael Zavelevich, and Daniil Gluzman. "VILLOUS LYMPHOCYTES IN BLOOD AND BONE MARROW IN SOME FORMS OF B-CELL LYMPHOID MALIGNANCIES." EUREKA: Life Sciences, no. 5 (September 30, 2020): 29–33. http://dx.doi.org/10.21303/2504-5695.2020.001429.
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The cytological and immunocytochemical features of the lymphocytes with villous morphology in peripheral blood and bone marrow in some B-lymphoproliferative disorders were studied. The diagnosis of hairy cell leukemia, a hairy cell leukemia variant, splenic marginal zone lymphoma and splenic diffuse red pulp small B-cell lymphoma was ascertained in accordance with the new revision of the WHO classification (2016). The neoplastic cells of hairy cell leukemia were determined by the presence of high tartrate resistant acid phosphatase (TRAP) activity. Cell surface expression of CD19, CD20 and CD21 antigens was detected. Also, the expression of CD25, CD103 and CD200, and in some cases cyclin D1, was found out. CD5, CD10 and CD23 were not detected. The immunophenotype of cells in splenic marginal zone lymphoma with villous processes also corresponded to the mature B cells. The expression of CD19, CD20 and CD21 was observed in all cases, CD11c – in 50% of patients, CD25 or CD5 – in 10% of patients. In 80% of patients, the pathologic cells did not show TRAP activity. In the bone marrow and peripheral blood cells of patients with diffuse red pulp lymphoma, TRAP activity was not detected. An immunophenotype in the hairy cell leukemia variant was different from those of classic HCL (CD19+CD20+CD22+CD103+CD11c+CD5–CD10–CD23–). Characterized immunophenotypical markers, which have differential diagnostic values in several forms of lymphoid tumors of B cell origin, will be important for the choice of treatment methods and prognosis
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Rymkiewicz, Grzegorz, Renata Woroniecka, Katarzyna Blachnio, Barbara Pienkowska-Grela, and Jan Walewski. "Flow Cytometry and Fluorescence In Situ Hybridization Are Methods of Choice for Routine Diagnosis of Mantle Cell Lymphoma." Blood 106, no. 11 (November 16, 2005): 4659. http://dx.doi.org/10.1182/blood.v106.11.4659.4659.
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Abstract Mantle cell lymphoma (MCL) is a distinct clinicopathologic entity, characterized by expansion of lymphocytes with co-expression of CD5 and CD20 and frequent t(11;14) translocation. MCL and its morphological variants are frequently confused with other lymphoma subtypes. The aim of this study was to analyze a contribution of histopathology (HP), immunohistochemistry (IHC), flow cytometry (FCM) and cytogenetic analysis with fluorescence in situ hybridization (FISH) to ultimate diagnosis of MCL. We identified 66 pts diagnosed with MCL either by use of HP/IHC or/and FCM. Initial diagnosis was based on HP/IHC only, and was validated in 55 of 66 patients by combined use of HP/IH, FCM, and FISH. We examined paraffin sections IHC panel consisting of antibodies to CD3, CD5, CD20, CD23, CD43, and cyclin D1. FCM analysis was done by 3-colour direct immunofluorescence with extended panel of antibodies to CD5, CD10, CD11c, CD19, CD20, CD22, CD23, CD25, CD38, CD45, HLADR, FMC7, light and heavy chains. We used FISH to detect the t(11;14) in interphase cells of 24 cases of MCL. All 55 cases of MCL were CD20 positive and CD23 negative on IHC, 32 of 51 (63%) and 46 of 52 (88%) cases coexpressed the CD5 and CD43 antigens, respectively. Cyclin-D1 staining revealed nuclear positivity in 38 of 52 (73%) pts. Dual expression of CD5 and cyclin D1 - a finding highly reliable for MCL diagnosis on IHC, was seen in 49% (27/55) of pts. All MCL cases were CD20 (51/51) and CD19 (55/55) positive by FCM with higher intensity of CD20 expression compared to CD19 in 100% (51/51) of cases. CD5 and CD25 were coexpressed in 54 of 55 (98%) and in 43 of 49 (88%) pts respectively. CD22 (45/45) and HLADR (55/55) were positive in all cases. FMC7 and CD38 were found in 22 of 23 (96%) and in 19 of 23 (83%) patients, respectively. CD10, CD11c, CD23 were only seen on a subpopulation of cells with weak intensity in 15%(7/48), 13% (6/45), and 11% (5/46) pts., respectively. MCL cells expressed moderate intensity monoclonal surface light chains in 47 of 52 (90%) pts with L light chain predominance and IgM+/IgD+ in 16 of 17 (94%) pts. False or incomplete initial diagnosis based mainly on lymph node HP/IHC was found in 35 of 66 (53%) cases. False FCM diagnosis of MCL was found in 2 of 66 (3%) cases. Results of FCM and FISH were consistent with the MCL diagnosis in 92% (22/24) of patients, in our hands. Our data indicate that the phenotypic pattern of MCL by FCM is remarkably constant among patients. As MCL represents a frequent diagnostic challenge, a combined use of FCM and FISH may provide an optimum solution.
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Paiva, Aldair Sousa, Alessandra Suelen Jardim Silva, Victor lima Soares, Gustavo Henrique de Medeiros Oliveira, Lenilton Silva DA Silva Júnior, Hugo Henrique de Freitas Ferreira, Rodrigo Villar Freitas, et al. "Importance of Flow Cytometry in the Differential Diagnosis of Hairy Cell Leukemia in the State of Rio Grande Do Norte, Brazil." Blood 136, Supplement 1 (November 5, 2020): 14–15. http://dx.doi.org/10.1182/blood-2020-143225.
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Introduction:Hairy Cell Leukemia (HCL) is a B-cell non-Hodgkin's Lymphoma (B-NHL) representing about 2% of chronic leukemias, is manifested in adults with an average age of 55 years old or more and the ratio of male: female is 5:1, being more common among white people. It is characterized by the presence of neoplastic lymphocytes with cytoplasmic projections (villous cells), a characteristic commonly observed in other DLPCs such as variant HCL (HCL-v) and splenic villous cell lymphoma (SVCL), being the immunophenotyping by flow cytometry determinant in the differential diagnosis of these neoplasms. HCL is characterized by splenomegaly, hepatomegaly, pancytopenia in peripheral blood (PB) with leukopenia, anemia, neutropenia, monocytopenia, and thrombocytopenia. It has a low number of circulating tumor cells, spleen, liver, and bone marrow (BM) infiltration.Objective:To investigate, by flow cytometry, patients with lymphocytosis and presence of villous lymphocytes in the characterization of HCL and HCV-v and SMZL.Methodology:Were investigated samples of peripheral blood (SP) and bone marrow (MO) from 27 patients previously diagnosed with DLPC and presence of villous lymphocytes which were by flow cytometry with a panel of monoclonal antibodies (MoAb) conjugated to fluorochromes and targeted to T-lymphocytes: CD1a, CD2, CD3, CD5, CD7, subpopulation T-helper (CD3/CD4) and T-cytotoxic (CD3/CD8), in addition to TCR a/b and TCR g/d; Natural Killer cells: CD16-56; B-lymphocytes: CD19, CD20, CD21, CD22, CD23, CD79b, CD200, IgM, IgG, IgD, anti-kappa and anti-lambda, in addition to CD10, TdT (Terminal deoxynucleotidyl Transferase), CD103, CD123, CD11c, CD25, CD38, CD138, CD45 and CD14. At the same time, a complete blood count with differential white blood cell count and investigation of clinical and demographic data such as age, sex and ethnicity / race were also performed.Results:The distribution of patients according to ethnicity and gender, there was a predominance of white individuals and males. The age group most affected was in patients older than 60 years. All patients expressed pan-B antigens on leukemic cells with expression of CD19, CD22 / CD20 (Forte), sIgH, associated with clonal restriction for immunoglobulin light chain (kappa= 20 and lambda= 7), associated with FMC7 expression, HLADR, CD38 and CD45 strong and negativity to CD10, CD138, CD200, CD23, CD5, TdT and related T antigens. Sixteen cases were categorized as HCL, six HCLv and five SVCL. The immunophenotyping of HCL cases was positive for CD103, CD25, CD123 and CD11c. HCLv was negative for CD103 in three cases and CD25 and SVCL negative for CD103, CD123 and CD11c and CD25 in all cases.Conclusions:The precise diagnosis of HCL has fundamental importance because each NHL-B has a specific treatment, besides emphasizing the sensitivity and speed of the IFC regarding diagnosis and follow-up. Disclosures No relevant conflicts of interest to declare.
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Jung, Georges, Sylvie Thiebault, Jean-Claude Eisenmann, Eckart Wunder, Marie Haas, Yasid Arkam, Mario Ojeda-Uribe, and Philippe Henon. "Quantitative Phenotyping and Discriminant Analysis Improve Scoring Classification in Late B-Lymphoproliferative Disorders." Blood 106, no. 11 (November 16, 2005): 1463. http://dx.doi.org/10.1182/blood.v106.11.1463.1463.
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Abstract Multivariate analysis classification of chronic lymphocytic leukemia (CLL) and lymphoma (non-CLL) disorders is investigated in 299 patients by an extended panel of surface markers, and compared with Matutes classical scoring proposal. Diagnosis was based on clinical features, cell morphology, node or bone marrow histology, and immunological scoring system. Results are obtained on directly labeled tumoral cells by flow cytometry gating. Patients included 154 CLL, 2 Richter transformation, and 143 lymphoma (26 follicular, 49 lymphocytic, 18 other low-grade, 7 Waldenström macroglobulinemia, 13 mantel, 11 diffuse large-cell, 6 Burkitt, 4 marginal zone-cell, 5 hairy-cell leukemia, 2 MALT, 1 prolymphocytic leukemia, 1 SLVL). For CD43, FMC7, CD23, CD5, CD79b (% stained cells) and CD20, CD22 surface antigen intensities Chi-Square values indicate very high probability of correct classification (varing from 621 to 94.9; p<0.0000). If, alternatively, % of CD22, CD20, CD19 and intensities of CD79b, CD5, CD19, CD43, CD23 and kappa/lamba chains are employed, Chi-Square yields values of lower significance (varing from 65 to 0.1; p<0.0000 to 0.6573). Using classical panel scoring with CD79b, 82.4 % of patients were correctly classified, compared to 84.5% after replacing CD79b by CD22 intensity. If CD43 is added, correct classification increased to 89.6% and 88.1% of patients, respectively; this improvement is due to better allocation of CLL. In discriminant analysis 91.3% of patients are correctly classified with the panel including CD79b, and 90.9% with CD22 intensity. CD43 enhances the allocation of either one to 94.3%. Using our previous discriminant analysis with CD79b (Jung G, et al. Br J Haematol.2003; 120:496–499), this blind analysis correctly classified the population in 87.1%, compared to 91.3% with the new one. By adding CD43, it moved from 92.4% up to 94.3%. In order to find the optimal combination of the selected best markers, a stepwise probit discrimination was performed. Using CD43 and FMC7 yields a correct classification of 90.3%; after addition of CD5, CD79b, CD23, and CD22 intensity, efficiency increased to 94.6%. Further added markers don’t improve classification. Efficiency of this panel was further confirmed by hierarchical cluster and principal components analysis. Cluster analysis with squared Euclidian distances separated CLL from non-CLL patients with low overlaps: 86.6% of cases are correctly identified. Separated points in the plot representing patients with CLL and non-CLL, obtained by principal components analysis of surface markers, confirm the high predictive potential of this panel. The same analysis of surface marker positions for non-CLL suggests use of: % of CD79b, FMC7, and CD22 intensity, and for CLL: % of CD5, CD23, CD43. So, the addition of CD43 improves as well the discriminant function as the scoring system. Our selected panel of best markers is useful in distinguishing CLL from non-CLL and offers a better distinction by discriminant analysis. Furthermore quantitative expression of each marker and its predictive value improve diagnosis and classification.
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Matutes, E., R. Morilla, K. Owusu-Ankomah, A. Houlihan, and D. Catovsky. "The immunophenotype of splenic lymphoma with villous lymphocytes and its relevance to the differential diagnosis with other B-cell disorders." Blood 83, no. 6 (March 15, 1994): 1558–62. http://dx.doi.org/10.1182/blood.v83.6.1558.1558.
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Abstract Splenic lymphoma with villous lymphocytes (SLVL) is a low-grade disorder that regularly presents with peripheral blood involvement. We describe the immunophenotype of the circulating cells from 100 SLVL patients whose disease has been characterized on clinical, morphologic, and histologic grounds. Cells from all cases expressed B-cell antigens (CD19 and CD37) and/or HLA-Dr and showed light chain restriction (kappa/lambda: 1.5/1) with moderate to strong intensity of membrane Ig staining. Cells from most cases (> 80%) were CD24+, FMC7+, and expressed strongly membrane CD22. The monoclonal antibodies CD10, CD23, and CD38 were positive in one-third of the cases; CD11c in 47%; and CD25 in 25% of cases. A minority of cases (< 20%) were positive with HC2, B-ly-7, and CD5. However, none of the 19 CD5+ cases had the phenotype characteristic of chronic lymphocytic leukemia (CD5+, CD23+, FMC7-, weak surface Ig and membrane CD22). None of the 17 CD25+ cases had the immunophenotype typical of hairy cell leukemia (CD25+, CD11c+, HC2+, B-ly-7+). HC2 and B-ly-7 were the most useful reagents to distinguish SLVL from hairy cell leukemia. Our findings demonstrate that SLVL has a distinct immunologic profile and that monoclonal antibodies are important for the differential diagnosis between this disease and other B-lymphoproliferative disorders with which SLVL can be confused.
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Matutes, E., R. Morilla, K. Owusu-Ankomah, A. Houlihan, and D. Catovsky. "The immunophenotype of splenic lymphoma with villous lymphocytes and its relevance to the differential diagnosis with other B-cell disorders." Blood 83, no. 6 (March 15, 1994): 1558–62. http://dx.doi.org/10.1182/blood.v83.6.1558.bloodjournal8361558.
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Splenic lymphoma with villous lymphocytes (SLVL) is a low-grade disorder that regularly presents with peripheral blood involvement. We describe the immunophenotype of the circulating cells from 100 SLVL patients whose disease has been characterized on clinical, morphologic, and histologic grounds. Cells from all cases expressed B-cell antigens (CD19 and CD37) and/or HLA-Dr and showed light chain restriction (kappa/lambda: 1.5/1) with moderate to strong intensity of membrane Ig staining. Cells from most cases (> 80%) were CD24+, FMC7+, and expressed strongly membrane CD22. The monoclonal antibodies CD10, CD23, and CD38 were positive in one-third of the cases; CD11c in 47%; and CD25 in 25% of cases. A minority of cases (< 20%) were positive with HC2, B-ly-7, and CD5. However, none of the 19 CD5+ cases had the phenotype characteristic of chronic lymphocytic leukemia (CD5+, CD23+, FMC7-, weak surface Ig and membrane CD22). None of the 17 CD25+ cases had the immunophenotype typical of hairy cell leukemia (CD25+, CD11c+, HC2+, B-ly-7+). HC2 and B-ly-7 were the most useful reagents to distinguish SLVL from hairy cell leukemia. Our findings demonstrate that SLVL has a distinct immunologic profile and that monoclonal antibodies are important for the differential diagnosis between this disease and other B-lymphoproliferative disorders with which SLVL can be confused.
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Kuvshinov, Aleksei, Sergei Voloshin, Irina Martynkevich, Ludmila Martynenko, Andrei Garifullin, Elizaveta Kleina, and Kudrat Abdulkadyrov. "Phenotypic Characteristics of Tumor Cells in Patients with Chronic Lymphocytic Leukemia into Different Prognostic Groups." Blood 126, no. 23 (December 3, 2015): 5276. http://dx.doi.org/10.1182/blood.v126.23.5276.5276.
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Abstract Background. The presence or absence of certain cluster of differentiation on the tumor cells of chronic lymphocytic leukemia may affect the course of the disease. Influence of genetic abnormalities on the prognosis of the disease was also proved. Aim. To determine the relationship of the phenotype of tumor cells with genetic prognostic groups of patients with chronic lymphocytic leukemia (CLL). Methods. Thirty-five adult pts (median age 61 year, range 44 - 82; male 24, female 11) with diagnosed CLL were included in the study. The CLL was diagnosed according to the standard basic examination (complete blood count with differential, multicolor flow cytometry (MFC) of blood and bone marrow (BM), lymph node and BM immunohistochemistry (IHC), computered tomography). Cytogenetic studies were performed on blood samples using standard GTG-method. Interphase FISH analyses were performed according to the manufacturer's protocol using DNA probes: LSI 13(RB1)13q14, LSI ATM (11q22), CEP12, LSI TP53 (17p13.1) (Abbott). Immunophenotype (IFT) of CLL cells assessed with combinations: CD3/CD19, CD19/CD5, CD19/CD11c, CD19/CD20, CD19/CD22, CD19/CD23, CD19/CD25, CD19/CD38, CD19/CD43, CD19/CD81, CD19/HLA-DR, and CD19/CD5/CD23. Results. Stratification of patients into prognostic groups was performed based on identified GA. Favorable prognosis - patients with del(13q) (n = 9); neutral prognosis - normal karyotype (n = 14) or trisomy of chromosome 12 (n = 4); unfavorable prognosis - del(17p) (n = 3), del(11q) (n = 3) and the complex karyotype (n = 2). Expression of CD20 was lower, and CD38 - higher in adverse group (51.0±16.31 % and 36.02±10.35 %, respectively) versus neutral or favorable groups (CD20+ - 83.17±5.52 % and 84.41±4.7 %; CD38 - 10.46±4.8 %, and 12.44±4.1 %, respectively, p <0.05). The expression level of CD20 and CD38 did not differ between the neutral and favorable groups. The number of patients with CD38 expression more than 10% was higher in the unfavorable group (7/8) versus favorable (4/8) (p <0.05). At the same time overexpression of CD38 was observed more frequently in patients with a lack of expression of CD23 on CD5 tumor cells (CD5+CD23-) (p<0.05). Expression of HLA-DR was higher in patients with MRD-negative remissions (3/4) versus patients with MRD-positive remissions (1/8) (p<0.05). Conclusions. The study of the influence of various factors on the prognosis and course of CLL requires a comprehensive approach. Further researches are needed to determine the relationship between CLL affecting factors like genetic abnormalities, phenotypic characteristics of the tumor cells and MRD. Disclosures No relevant conflicts of interest to declare.
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Gupta, Gaurav K., Xiaoping Sun, Constance M. Yuan, Maryalice Stetler-Stevenson, Robert J. Kreitman, and Irina Maric. "Usefulness of Dual Immunohistochemistry Staining in Detection of Hairy Cell Leukemia in Bone Marrow." American Journal of Clinical Pathology 153, no. 3 (October 28, 2019): 322–27. http://dx.doi.org/10.1093/ajcp/aqz171.
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Abstract Objectives We evaluated efficacy of two dual immunohistochemistry (IHC) staining assays in assessing hairy cell leukemia (HCL) involvement in core biopsies and compared the results with concurrently collected flow cytometric data. Methods Overall, 148 patients with HCL (123 male, 25 female; mean age: 59.8 years; range: 25-81 years) had multiparameter flow cytometry performed using CD19, CD20, CD22, CD11c, CD25, CD103, CD123, surface light chains, CD5, and CD23. In parallel, bone marrow IHC was done using PAX5/CD103 and PAX5/tartrate-resistant alkaline phosphatase (TRAP) dual IHC stains. Results Overall sensitivity of dual IHC stains was 81.4%, positive predictive value was 100%, and negative predictive value was 81.7%. All IHC-positive cases concurred with flow cytometry data, even when HCL burden was extremely low in the flow cytometry specimens (as low as 0.02% of all lymphoid cells). Conclusions Dual IHC stain is a sensitive tool in detecting HCL, even in cases with minimal disease involvement.
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Frank, Robin R., Sucheta Jagan, Laura A. Paganessi, Melissa L. Larson, Reem Karmali, Parameswaran Venugopal, Stephanie A. Gregory, and Kent W. Christopherson. "CD20, CD22, CD23, but Not CD37 Expression on CD19+ B-Cells Is Altered by Exogenous Factors in a Sub-Population of Chronic Lymphocytic Leukemia/Small Lymphocytic Leukemia (CLL/SLL) Patients,." Blood 118, no. 21 (November 18, 2011): 3685. http://dx.doi.org/10.1182/blood.v118.21.3685.3685.
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Abstract Abstract 3685 Introduction: Chronic Lymphocytic Leukemia/Small Lymphocytic Leukemia (CLL/SLL) is a lymphoproliferative disorder that is characterized by the slow accumulation of malignant B cells. Patients follow heterogeneous clinical courses. The effectiveness of Rituximab, an anti-CD20 monoclonal antibody (mAb), is limited because target B cells from CLL patients express low levels of CD20. We previously reported that human serum suppresses CD20 expression ex vivo. Therefore, understanding mechanisms of low expression of CD20 as well as other target surface receptors would benefit CLL patients. New therapies such as epratuzumab (anti-CD22 mAb), lumiliximab (anti-CD23 mAb), and TRU-016 (anti-CD37 SMIP protein) are being investigated as alternative means to treat CLL. We therefore investigated CD20, CD22, CD23, and CD37 expression during ex vivo culture of CLL B cells from thirteen patients with and without human serum albumin (HSA), normal donor serum (NS), autologous CLL serum (CS), fetal bovine serum (FBS), IL2, IL4, IL13, IL15, IL21, TNFα, IFNα, IFNγ, G-CSF, or GM-CSF. Methods: Peripheral blood (PB) from thirteen CLL patients and five healthy normal donors was obtained with IRB approval. Nine CLL patients were Rai 0/1, one Rai 4, and three unknown. Prognosis, as determined by cytogenetics and/or FISH, was: four good, three intermediate, one poor, and five unknown. Beta-2 Microglobulin (B2M) ranged from 1.4–7.1 mg/L. CD19+ cells, isolated by positive magnetic selection, were cultured in AIM-V serum-free media at 37°C, 5% CO2, 100% humidity for 0, 24, 48, and 96 hours. Cells were either untreated, treated with 5% serum, or 5ng/mL cytokine. Receptor expression was measured by multivariate flow cytometry and calculated as percent loss or increase in response to treatment. Data was presented as mean ± SEM and analyzed using the Mann-Whitney U test as compared to HSA treatment. Results: Prior to culture, CD19+ CLL cells had 11.7±1.7% CD20, 40.3±7.9% CD22, 60.6±6.8% CD23, and 81.6±2.7% CD37 positive expression (N=13). Analysis of untreated CLL cells cultured for 96 hours showed that the CLL patients subdivided into two groups based on changes in CD20 expression: variable (72.5±7.4% CD20+, N=9) and stable (27.2±4.2% CD20+, N=4). Within the variable group, losses in CD20 expression resulted from treatment as compared to HSA were: NS (40.2±3.6%, p<0.05), CS (43.6±8.8%, p<0.05), FBS (37.2±5.0%, p=0.064), IL2 (11.5±5.1%, p=0.860), IL4 (33.3±8.9%, p=0.185), and IL13 (24.2±9.1%, p=0.596). The percent loss in CD20 expression due to IL4 was significantly greater than IL2 (p<0.05). Percent losses in CD22 expression were: NS (62.4±9.4%, p<0.05), CS (63.2±8.1%, p<0.05), and FBS (66.6±6.8%, p<0.05). No loss in CD37 expression was significant. Percent increases in CD23 expression were: IL4 (253.7±79.4%, p=0.930) and IL13 (86.7±77.9%, p=0.377). Within the stable group after treatment, percent losses in CD22 were: IL2 (40.0±10.1%, p=1.000) and IL4 (29.1±6.5%, p=0.114). Percent increase in CD37 expression was: FBS (53.3±18.3%, p<0.05). Conclusions: Our findings show that cells from CLL patients form groups based on the ability of cells to maintain low CD20 expression after serum-free culture for 96 hours: variable and stable. Only CLL cells within the variable group have a high upregulation of CD20. These patient samples respond to serum through a reduction of CD20. In addition, suppression of CD20 expression due to IL4 or IL13 treatment was similar to that of serum. Both IL4 and IL13 share a common receptor that signals through the JAK/STAT pathway, suggesting downstream signals may be responsible for suppression of CD20 expression in CLL. Similarly, CLL patients belonging to the variable group also have reduced expression of CD22 in response to serum. Loss of CD23 expression in CLL cells cultured over time, in the absence of IL4 or IL13 treatment, may be predictive of poor clinical outcomes in patients treated with the anti-CD23 monoclonal antibody. CD20, CD22, and CD23 are susceptible to environmental cues, whereas expression of CD37 remained high throughout culture and independent of treatment. As a result, we predict CD37 to be a good target for treating CLL due to its stability. Ongoing clinical trials with TRU-016 or other agents that specifically target CD37 may therefore be of potential therapeutic benefit. Disclosures: No relevant conflicts of interest to declare.
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Newman, RA, B. Peterson, FR Davey, C. Brabyn, H. Collins, VL Brunetto, DB Duggan, RB Weiss, I. Royston, and FE Millard. "Phenotypic markers and BCL-1 gene rearrangements in B-cell chronic lymphocytic leukemia: a Cancer and Leukemia Group B study." Blood 82, no. 4 (August 15, 1993): 1239–46. http://dx.doi.org/10.1182/blood.v82.4.1239.1239.
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Abstract The markers, CD11b, CD11c, CD14, CD21, CD23, CD25, CD38, and FMC7 were correlated with morphologic and other laboratory and clinical characteristics of 127 patients with untreated CD5+ chronic lymphocytic leukemia (CLL). Only CD38 and CD21 were significantly associated with atypical CLL morphology. The integrin associated markers CD11b and CD11c were associated with lower leukocyte count (white blood cell count [WBC]) and lower Rai stage. By contrast, the activation antigen CD23 was associated with a higher WBC, higher Rai stage, younger age group, and the presence of lymphadenopathy. Therefore, we conclude that CD23 positivity may reflect a more aggressive form of CLL, and CD11b and CD11c positivity a less aggressive form. The BCL-1 gene rearrangement was present in 5 of 84 (6%) CLL cases examined and was associated with atypical morphology and surface expression of CD11b. Patients with a BCL-1 gene rearrangement may represent a CLL subset or possibly a different B-cell disease.
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Newman, RA, B. Peterson, FR Davey, C. Brabyn, H. Collins, VL Brunetto, DB Duggan, RB Weiss, I. Royston, and FE Millard. "Phenotypic markers and BCL-1 gene rearrangements in B-cell chronic lymphocytic leukemia: a Cancer and Leukemia Group B study." Blood 82, no. 4 (August 15, 1993): 1239–46. http://dx.doi.org/10.1182/blood.v82.4.1239.bloodjournal8241239.
Full textAbstract:
The markers, CD11b, CD11c, CD14, CD21, CD23, CD25, CD38, and FMC7 were correlated with morphologic and other laboratory and clinical characteristics of 127 patients with untreated CD5+ chronic lymphocytic leukemia (CLL). Only CD38 and CD21 were significantly associated with atypical CLL morphology. The integrin associated markers CD11b and CD11c were associated with lower leukocyte count (white blood cell count [WBC]) and lower Rai stage. By contrast, the activation antigen CD23 was associated with a higher WBC, higher Rai stage, younger age group, and the presence of lymphadenopathy. Therefore, we conclude that CD23 positivity may reflect a more aggressive form of CLL, and CD11b and CD11c positivity a less aggressive form. The BCL-1 gene rearrangement was present in 5 of 84 (6%) CLL cases examined and was associated with atypical morphology and surface expression of CD11b. Patients with a BCL-1 gene rearrangement may represent a CLL subset or possibly a different B-cell disease.
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Chang, Heesoon, Yousang Gwack, Dior Kingston, John Souvlis, Xiaozhen Liang, Robert E. Means, Ethel Cesarman, Lindsey Hutt-Fletcher, and Jae U. Jung. "Activation of CD21 and CD23 Gene Expression by Kaposi's Sarcoma-Associated Herpesvirus RTA." Journal of Virology 79, no. 8 (April 15, 2005): 4651–63. http://dx.doi.org/10.1128/jvi.79.8.4651-4663.2005.
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ABSTRACT Epstein-Barr virus (EBV) EBNA2 and Kaposi's sarcoma-associated herpesvirus (KSHV) replication and transcription activator (RTA) are recruited to their responsive elements through interaction with a Notch-mediated transcription factor, RBP-Jκ. In particular, RTA and EBNA2 interactions with RBP-Jκ are essential for the lytic replication of KSHV and expression of B-cell activation markers CD21 and CD23a, respectively. Here, we demonstrate that like EBV EBNA2, KSHV RTA strongly induces CD21 and CD23a expression through RBP-Jκ binding sites in the first intron of CD21 and in the CD23a core promoter, respectively. However, unlike EBV EBNA2, which alters immunoglobulin μ (Igμ) and c-myc gene expression, RTA did not affect Igμ and c-myc expression, indicating that KSHV RTA targets the Notch signal transduction pathway in a manner similar to but distinct from that of EBV EBNA2. Furthermore, RTA-induced expression of CD21 glycoprotein, which is an EBV receptor, efficiently facilitated EBV infection. In addition, RTA-induced CD23 glycoprotein underwent proteolysis and gave rise to soluble CD23 (sCD23) molecules in B lymphocytes and KSHV-infected primary effusion lymphocytes. sCD23 then stimulated primary human lymphocytes. These results demonstrate that cellular CD21 and CD23a are common targets for B lymphotropic gammaherpesviruses and that KSHV RTA regulates RBP-Jκ-mediated cellular gene expression, which ultimately provides a favorable milieu for viral reproduction in the infected host.
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Srivastava, Bhaskar, William J. Quinn, Kristin Hazard, Jan Erikson, and David Allman. "Characterization of marginal zone B cell precursors." Journal of Experimental Medicine 202, no. 9 (October 31, 2005): 1225–34. http://dx.doi.org/10.1084/jem.20051038.
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Selection of recently formed B cells into the follicular or marginal zone (MZ) compartments is proposed to occur by way of proliferative intermediates expressing high levels of CD21/35 and CD23. However, we show that CD21/35high CD23+ splenocytes are not enriched for proliferative cells, and do not contribute substantially to the generation of follicular B cells. Instead, ontogenic relationships, steady-state labeling kinetics, and adoptive transfer experiments suggest that CD21/35high CD23+ splenocytes serve primarily as precursors for MZ B cells, although their developmental potential seems to be broader and is influenced by environmental cues that are associated with lymphopenia. Furthermore, CD21/35high CD23+ splenocytes share several key functional characteristics with MZ B cells, including their capacity to trap T-independent antigen and a heightened proliferative response to LPS. These observations challenge previous models of peripheral B cell maturation, and suggest that MZ B cells develop by way of CD21/35high CD23+ intermediates.
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Patuzzo, Giuseppe, Filippo Mazzi, Antonio Vella, Riccardo Ortolani, Alessandro Barbieri, Elisa Tinazzi, Giacomo Marchi, et al. "Immunophenotypic Analysis of B Lymphocytes in Patients with Common Variable Immunodeficiency: Identification of CD23 as a Useful Marker in the Definition of the Disease." ISRN Immunology 2013 (April 4, 2013): 1–8. http://dx.doi.org/10.1155/2013/512527.
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Common variable immunodeficiency (CVID) is a primary immunodeficiency characterized by the failure of B lymphocytes differentiation leading to deficient immunoglobulins secretion. The identified genetic defects account only for a minority of cases. The importance of B cells immunophenotyping in the classification of CVID is known. This procedure can identify alterations on the cell surface molecules expression that could explain some immunological disorders characteristic of CVID. Moreover, some immunophenotypical aspects can correlate with clinical features of the disease. We used this procedure to analyze a cohort of 23 patients affected by CVID, in order to identify the novel alterations of B cells and to find the possible correlations with clinical features. Circulating B cells were studied by flow cytometry incubating whole blood with specific antibodies for B cell surface molecules including CD27, IgM, IgD, CD21, and CD23. We compared the population of “switched memory” IgD− CD27+ B lymphocytes with the population of “switched memory” IgM− IgD− CD23− CD27+ B cells. These last B cells were reduced in patients compared to healthy controls; moreover, IgM− IgD− CD23− CD27+ B cells were lower than IgD− CD27+ B cells in patients with CVID. The reduction of this subset of B lymphocytes correlates more tightly than IgD− CD27+ B cells with lymphadenopathy and airways infections. In conclusion, our findings may help in better identifying patients with CVID.
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White, Lindsey J., Bradford W. Ozanne, Pierre Graber, Jean-Pierre Aubry, Jean-Yves Bonnefoy, and William Cushley. "Inhibition of Apoptosis in a Human Pre-B–Cell Line by CD23 Is Mediated Via a Novel Receptor." Blood 90, no. 1 (July 1, 1997): 234–43. http://dx.doi.org/10.1182/blood.v90.1.234.
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Abstract Human CD23 is a 45-kD type II membrane glycoprotein, which functions as a low-affinity receptor for IgE and as a ligand for the CD21 and CD11b/CD11c differentiation antigens. CD23 is released from the surface of cells as soluble fragments, and a 25-kD species of soluble CD23 (sCD23) appears to act as a multifunctional cytokine. In this report, sCD23 is shown to sustain the growth of low cell density cultures of a human pre-B–acute lymphocytic leukemia cell line, SMS-SB: no other cytokine tested was able to induce this effect. Flow cytometric analysis indicates that sCD23 acts to prevent apoptosis of SMS-SB cells. SMS-SB cells cultured at low cell density possess low levels of bcl-2 protein. Addition of sCD23 to cells at low cell density maintained bcl-2 expression at levels equivalent to those observed in SMS-SB cells cultured at higher cell densities. No CD23 mRNA was found in SMS-SB cells, ruling out an autocrine function for CD23 in this cell line model. Although SMS-SB cells do not express the known receptors for CD23, namely CD21, CD11b-CD18, or CD11c-CD18, the cells specifically bind CD23-containing liposomes, but not glycophorin-containing liposomes. Binding of CD23-containing liposomes is inhibited by anti-CD23 but not by anti-CD21 or anti-CD11b/c monoclonal antibodies. The data show that sCD23 prevents apoptosis of the SMS-SB cell line by acting through a novel receptor.
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White, Lindsey J., Bradford W. Ozanne, Pierre Graber, Jean-Pierre Aubry, Jean-Yves Bonnefoy, and William Cushley. "Inhibition of Apoptosis in a Human Pre-B–Cell Line by CD23 Is Mediated Via a Novel Receptor." Blood 90, no. 1 (July 1, 1997): 234–43. http://dx.doi.org/10.1182/blood.v90.1.234.234_234_243.
Full textAbstract:
Human CD23 is a 45-kD type II membrane glycoprotein, which functions as a low-affinity receptor for IgE and as a ligand for the CD21 and CD11b/CD11c differentiation antigens. CD23 is released from the surface of cells as soluble fragments, and a 25-kD species of soluble CD23 (sCD23) appears to act as a multifunctional cytokine. In this report, sCD23 is shown to sustain the growth of low cell density cultures of a human pre-B–acute lymphocytic leukemia cell line, SMS-SB: no other cytokine tested was able to induce this effect. Flow cytometric analysis indicates that sCD23 acts to prevent apoptosis of SMS-SB cells. SMS-SB cells cultured at low cell density possess low levels of bcl-2 protein. Addition of sCD23 to cells at low cell density maintained bcl-2 expression at levels equivalent to those observed in SMS-SB cells cultured at higher cell densities. No CD23 mRNA was found in SMS-SB cells, ruling out an autocrine function for CD23 in this cell line model. Although SMS-SB cells do not express the known receptors for CD23, namely CD21, CD11b-CD18, or CD11c-CD18, the cells specifically bind CD23-containing liposomes, but not glycophorin-containing liposomes. Binding of CD23-containing liposomes is inhibited by anti-CD23 but not by anti-CD21 or anti-CD11b/c monoclonal antibodies. The data show that sCD23 prevents apoptosis of the SMS-SB cell line by acting through a novel receptor.
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Cro, Lilla, Andrea Ferrario, Nadia Zucal, Umberto Gianelli, Sonia Fabris, Lucia Nobili, Barbara Olivero, Francesca G. Rossi, Luca Baldini, and Giorgio Lambertenghi Deliliers. "Diagnostic Role of Flow Cytometry Analysis of Bioptical Samples in the Diagnosis of Lymphoid Tumors." Blood 112, no. 11 (November 16, 2008): 5286. http://dx.doi.org/10.1182/blood.v112.11.5286.5286.
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Abstract We reviewed flow cytometric immunophenotyping (FCI) data of 470 tissue suspensions suspected of being involved by lymphoma (371 lymph nodes, 263 surgical biopsies and 108 fine needle aspirations,16 spleens, 6 tonsils, and 77 other tissues) and we have compared corresponding histologic diagnosis. The screening panel of FCI (CD45, CD19, CD3, CD4, CD8, and sIgκ/sIgλ ratio) identified three main groups: 239 cases with demonstrable light chain restriction (sIgκ/sIgλ ratio ≤ 0.5 or ≥4); 37 cases with demonstrable T cell proliferation and polyclonal B cell population; 194 cases with polyclonal B cell and normal T cell populations (146 cases) or with not detectable CD45 reactivity and other leucocyte markers (48 cases). In group 1, 235 cases were then evaluated by means of the following markers: CD5, CD10, CD11a, CD11c, CD20, CD22, CD23, CD30, CD38, CD43, CD79a–b, CD103, CD138, FMC7, and, in group 2, 30 cases were evaluated by means of the following markers: CD1a, CD2, CD5, CD7, CD16, CD26, CD43, CD56, CD57, CD45RA/RO, anti-TCR-ab gd. The complete analysis identified in group 1 four main diagnostic subsets: A (26 cases) characterized by CD5+, CD23+/±, sIg dim (CLL-like); B (36 cases) characterized by CD5+, sIg bright (MCL/CLLv); C (89 cases) characterized by heterogeneous expression of Ig, CD20 and CD43 (lymphoproliferative syndromes CD5−, excluding hairy cell leukemia); D (84 cases) characterized by CD10+, CD20 bright, CD43− (follicular NHL like). In cluster B, FISH analysis for t(11;14) resulted positive in 15/27 cases; in cluster D, FISH analysis for t(14;18) resulted positive in 60/60 cases. Histologic analysis convalidated FCI data in 23 cases of subset A (88%), in 29 cases of subset B (80%) and in 60 cases of subset D (71%). Subset C included 39 cases of LCL and 15 cases of MZL. In group 2, all cases studied expressed an aberrant T phenotype but, with the exception of 1 case of NK proliferation, 1 case of likely Sezary syndrome/Micosis Fungoides (CD4+CD7−CD26−) and 1 case of T lymphoblastic lymphoma (CD3cy+TdT+), in the other 34 cases was not possible identify other peculiar subset. In this group, histologic analysis included 19 cases of NHL T (63%). Considering NHL vs no NHL, sensibility (SE) and specificity (SP) of FCI analysis resulted 88% and 92%, respectively; positive predictive value (PPV) was 96% and negative predictive value (NPV 78%). Considering B-cell NHL only, SE was 91%, SP 95%, PPV 97% and NPV 84%. Even if histology is the basis for the diagnosis of lymphoid tumors, however our study supports that FCI can play an important role mainly in B-NHL diagnosis, combining rapidity of analysis with a multiparametric analysis, also in presence of size limitated samples.
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Guo, CB, A. Kagey-Sobotka, LM Lichtenstein, and BS Bochner. "Immunophenotyping and functional analysis of purified human uterine mast cells." Blood 79, no. 3 (February 1, 1992): 708–12. http://dx.doi.org/10.1182/blood.v79.3.708.708.
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Abstract Human mast cells have been purified from uterine tissues, and their surface marker profile and function have been evaluated as part of ongoing studies of mast cell heterogeneity. Using a panel of antibodies, purified uterine mast cells (UMC; 81% +/- 7% purity, n = 10) were analyzed by immunofluorescence and flow cytometry for surface expression of various antigens. Consistent with previous analyses of mast cells from other tissues, UMC expressed HLA class I, IgE, c-kit receptor, CD9, CD33, CD43, CD45, and CD54, while CD11a, CD11b, CD14, CD16, CD23, and CD64 were not detected. Unlike other mast cells, UMC expressed CD11c/CD18 (p150,95) and CD32 (Fc gamma RII). Additional antigens not previously studied on mast cells included the selectin LECAM-1 (Leu-8) and several beta 1 and beta 3 integrins; expression of very late activation antigen-4 (VLA-4) (CD49d/CD29), VLA-5 (CD49e/CD29), and the vitronectin receptor (CD51/CD61) was seen. Functional studies showed that treatment of human umbilical vein endothelial cells with interleukin-1 (5 ng/mL for 4 hours) resulted in a twofold to threefold increase in adhesiveness for UMC. Purification procedures did not alter histamine release responses to anti-IgE or the calcium ionophore A23187, and treatment of UMC with an anti-CD32 monoclonal antibody (IV.3) did not induce histamine release or alter anti-IgE-induced release. These data suggest that UMC may possess unique phenotypic characteristics, and support the concept of mast cell heterogeneity.
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Guo, CB, A. Kagey-Sobotka, LM Lichtenstein, and BS Bochner. "Immunophenotyping and functional analysis of purified human uterine mast cells." Blood 79, no. 3 (February 1, 1992): 708–12. http://dx.doi.org/10.1182/blood.v79.3.708.bloodjournal793708.
Full textAbstract:
Human mast cells have been purified from uterine tissues, and their surface marker profile and function have been evaluated as part of ongoing studies of mast cell heterogeneity. Using a panel of antibodies, purified uterine mast cells (UMC; 81% +/- 7% purity, n = 10) were analyzed by immunofluorescence and flow cytometry for surface expression of various antigens. Consistent with previous analyses of mast cells from other tissues, UMC expressed HLA class I, IgE, c-kit receptor, CD9, CD33, CD43, CD45, and CD54, while CD11a, CD11b, CD14, CD16, CD23, and CD64 were not detected. Unlike other mast cells, UMC expressed CD11c/CD18 (p150,95) and CD32 (Fc gamma RII). Additional antigens not previously studied on mast cells included the selectin LECAM-1 (Leu-8) and several beta 1 and beta 3 integrins; expression of very late activation antigen-4 (VLA-4) (CD49d/CD29), VLA-5 (CD49e/CD29), and the vitronectin receptor (CD51/CD61) was seen. Functional studies showed that treatment of human umbilical vein endothelial cells with interleukin-1 (5 ng/mL for 4 hours) resulted in a twofold to threefold increase in adhesiveness for UMC. Purification procedures did not alter histamine release responses to anti-IgE or the calcium ionophore A23187, and treatment of UMC with an anti-CD32 monoclonal antibody (IV.3) did not induce histamine release or alter anti-IgE-induced release. These data suggest that UMC may possess unique phenotypic characteristics, and support the concept of mast cell heterogeneity.
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Chuksina, J. J., E. V. Kataeva, and T. A. Mitina. "Features of immunophenotypic finding B-cell lymphoproliferative diseases by flow cytometry." Kazan medical journal 101, no. 1 (February 11, 2020): 145–52. http://dx.doi.org/10.17816/kmj2020-145.
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Aim. To assess the information content of conventional and additional immunophenotypic markers (CD200, CD305) in the differential diagnosis B-cell lymphoproliferative diseases by flow cytometry.
Methods. An immunophenotypic study using 4-color flow cytometry was performed in 204 patients with different variants of B-cell non-Hodgkin's lymphomas. The study material included peripheral blood and bone marrow. The expression of CD45, CD19, CD20, CD22, CD79b, CD79a, CD5, CD10, CD23, FMC7, CD43, CD38, CD11c, CD103, CD25, CD 200, CD 305, light chains of immunoglobulins (kappa/lambda) using monoclonal antibodies (Becton Dickinson, USA) was evaluated. The intensity of antigen expression was assessed using mean fluorescence intensity (y. e.).
Results. Conventional FMC7-positive expression revealed only half patients with different variants of leukemization of non-Hodgkin's lymphomas, whereas atypical positive expression of CD23 was observed in patients with marginal spleen lymphoma and follicular lymphoma in 27.3 and 28.6% of cases, respectively. In mantle cell lymphoma, expression of CD200 in B-cell was detected in a significantly smaller number of observations, accompanied by a significant decrease in the average intensity of CD200 fluorescence compared to B-cell chronic lymphocytic leukemia (B-CLL) cells. The mean fluorescence intensity (MFI) of CD305 in hairy cell leukemia is significantly higher than in splenic marginal zone lymphoma (SMZL) with villous lymphocytes.
Conclusion. Different levels of the information content of some conventional markers were revealed in differential immunophenotypic diagnosis of B-cell lymphoproliferative diseases by flow cytometry; the use of additional markers CD200 and CD305 was highly informative in differential diagnostics between different variants of B-cell lymphoproliferative diseases with similar immunophenotypic and morphological characteristics of lymphoid elements.
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Cornet, Edouard, Alice-Sophie Boucher, Véronique Salaun, Florence Truquet, Michele Malet, Dina Naguib, Françoise Galateau-Salle, and Xavier Troussard. "Incidence Of Atypical Chronic Lymphocytic Leukemia In 1819 Patients With B Chronic Lymphoproliferative Disorder." Blood 122, no. 21 (November 15, 2013): 1770. http://dx.doi.org/10.1182/blood.v122.21.1770.1770.
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Abstract Flow cytometry is the diagnostic tool of choice to study abnormal lymphoid population detected in peripheral blood by morphological analysis. The main diagnosed chronic lymphoproliferative disorder (CLPD) is chronic lymphocytic leukemia (CLL). In a significant number of cases, a B-CLPD non-CLL can be diagnosed. Further molecular and histological examinations are then compulsory to characterize such hematologic malignancies. The objective of this study was to determine the incidence of atypical CLL among all B-CLPD diagnosed by flow cytometry. We retrospectively studied the B-CLPD consecutively diagnosed at the hospital of Caen (Normandy, France) between 2000 and 2013. The diagnosis of B-CLPD was based on the detection by flow cytometry of circulating lymphoid abnormal B cells. Multiparametric flow cytometry included markers CD19, CD20, CD22, CD79b, CD5, CD10, CD23, CD43, FMC7, CD38 and light chains (kappa and lambda) of surface immunoglobulin. The diagnosis of CLL was based on the criteria defined by Hallek et al (Blood 2008). The non-CLL B-CLPD were then explored by molecular analyses driven by the phenotype of B-cells (overexpression of cyclin D1 in case of CD5+/CD10-/CD23- B-CLPD and BCL2-JH rearrangement in case of CD10+ B-CLPD). In addition, histological evidence was necessary to classify the B-CLPD non-CLL. 1819 B-CLPD were detected by flow cytometry. The distribution of B-CLPD was as follows: 1156 cases (64%) of CLL or immunophenotypic equivalent (leukemic phase of small lymphocytic lymphoma (SLL) and monoclonal B-cell lymphocytosis (MBL)), 297 cases (16%) of marginal zone lymphoma (MZL), 84 cases (5%) of mantle cell lymphoma (MCL), 39 cases (2%) of follicular lymphoma (FL), 26 cases (1%) of hairy cell leukemia (HCL), 13 cases (<1%) of diffuse large B-cell lymphoma (DLBCL), 9 cases (<1%) of Waldenstrom's macroglobulinemia (WM) and 3 cases (<1%) of B-cells prolymphocytic leukemia (B-PLL). 65 cases (4%) remained unclassified due to lack of histological and molecular data. 127 cases (7%) did not meet the diagnostic criteria of CLL established by Hallek et al but were classified as atypical CLL because of the detection of a clonal B-cell proliferation expressing CD5+ / CD23+ / CD43+ / CD10- / FMC7+ / CD79b+ with moderate or high intensity and light chain kappa or lambda with moderate or strong intensity (absence of molecular or histological argument of MZL or MCL was required). CD20 marker was highly expressed in 113 cases (89%) of atypical CLL. We particularly studied the 1532 cases (84%) of B-CLPD expressing CD5 (table). CD5+ CD23+ B-CLPD cases accounted for 1293 (84%) with 1153 cases of CLL, 13 cases of MCL and 127 cases of atypical CLL. CD5+ CD23- B-CLPD accounted for 239 cases (16%) with 72 cases of MCL, 158 cases of MZL, 4 cases of FL, 2 cases of WM, 2 cases of CD23- CLL and one case of B-PLL.CD5+ casesCD5+ CD23+ B-CLPDCD5+ CD23- B-CLPDTotalCLL115301153Atypical CLL1272129MCL137285MZL0158158FL044WM022B-PLL011Total12932391532 WHO classification of hematologic malignancies do not include atypical CLL as defined by a clonal proliferation of B-cells expressing CD5+, CD23+, cyclin D1- with no histological evidence of MZL or MCL, and which do not meet all the diagnostic criteria of CLL (Hallek et al, Blood 2008). This concept of atypical CLL, first described by Criel et al (BJH 1997), is particularly interesting, because such B-CLPD seems to have a different outcome as compared with CLL (Oscier et al, BJH 1997) and to have a different biological presentation with atypical morphology of CLL cells (Criel et al, BJH 1997), more frequent trisomy 12 (Matutes et al, BJH 1996) and a stronger intensity of CD20 (Ugo et al, Leuk Lymphoma 2006). Diagnosis of B-CLPD relies on a multidisciplinary approach combining morphological, immunophenotypic, molecular and histological analyses. Despite detailed information of these analyses, there are B-CLPD which remain unclassifiable according WHO classification, especially CD5 positive B-CLPD. The concept of atypical CLL seems to take all its meaning to help define such unclassifiable entities. Disclosures: No relevant conflicts of interest to declare.
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Weitzman, James, Monica Betancur, Laurent Boissel, Arthur P. Rabinowitz, and Hans Klingemann. "Variable Contribution of Different Monocloncal Antibodies to NK Cell-Mediated ADCC Against Primary CLL Cells." Blood 110, no. 11 (November 16, 2007): 4715. http://dx.doi.org/10.1182/blood.v110.11.4715.4715.
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Abstract Chronic Lymphocytic Leukemia (CLL) is characterized by the expression of the B-cell antigens CD19, 20 and 22, along with CD5 and CD23. These antigens make the malignant cells an ideal target for monoclonal antibody (mAb) therapy. Although the mechanism of action of mAbs is complex and not fully understood, one well-described action is antibody-dependent cellular cytotoxicity (ADCC). Binding of mAb to its target surface antigen initiates cytotoxicity through the interaction of the Fc portion of the mAb with the Fc receptor (FcR) on natural killer (NK) cells. This triggers release of perforin and granzymes from NK cells, and subsequent killing of the target cells. This study’s objectives were to measure ADCC of 4 different mAbs against primary CLL cells, and determine if cytotoxicity is dependent on antigen density. Methods: Mononuclear cells from 16 patients with untreated CLL were separated by density gradient separation and served as targets. The antigen density for CD20, 22 and 23 of each patient sample was quantified by flow cytometry. Effector cells for ADCC were NK-92 cells that do not express FcR, and a high affinity Fc receptor-expressing NK-92 variant (NK92.26.5) that also expresses inhibitory receptors (i.e. KIR). A fluourochrome-based flow cytometric assay determined ADCC by subtracting NK-92 induced cytotoxicity from NK-92.26.5 induced killing. Monoclonal antibodies tested were Rituximab (anti-CD20, Biogen/IDEC), Veltuzumab (anti-CD20, Immunomedics), Epratuzumab (anti-CD22, Immunomedics), and Lumiliximab (anti-CD23, Biogen/IDEC). Results: Mean ADCC of the four antibodies tested against 16 primary CLL cells were: 46.5% for Rituximab; 43.4% for Veltuzumab; 5.8% for Epratuzumab; 8.8% for Lumiliximab. Cytotoxicity of NK-92 and NK-92.26.5 against CLL cells without antibody ranged from 2–6%. Mean antigen density on the 16 CLL patient specimens were: CD20: 27,900 (range: 10,000–56,100); CD22: 820 (600–1300); CD23: 9870 (2340–14,800). Conclusions: We have developed a reliable in vitro assay to measure ADCC of mAbs against CLL cells. Our results indicate that ADCC contributes to cytotoxcity of CLL in vitro, and suggest that the magnitude of ADCC depends upon the surface antigen targeted. Anti-CD20 antibodies had significantly greater ADCC than the anti-CD22 and CD23 antibodies. This pattern was consistent in all patient cells tested. A similar pattern was observed with the surface antigen density on CLL cells tested, suggesting a correlation between cell surface antigen density and ADCC. Our results also suggest that resistance of primary CLL cells toward NK-mediated killing can be overcome by monoclonal antibodies even in the presence of inhibitory KIR expression on NK cells.
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Yap, Hooi-Yeen, Thin-Sam Siow, Sook-Khuan Chow, and Sin-Yeang Teow. "Epstein-Barr Virus- (EBV-) Immortalized Lymphoblastoid Cell Lines (LCLs) Express High Level of CD23 but Low CD27 to Support Their Growth." Advances in Virology 2019 (March 28, 2019): 1–9. http://dx.doi.org/10.1155/2019/6464521.
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Epstein-Barr virus (EBV) is one of the common human herpesvirus types in the world. EBV is known to infect more than 95% of adults in the world. The virus mainly infects B lymphocytes and could immortalize and transform the cells into EBV-bearing lymphoblastoid cell lines (LCLs). Limited studies have been focused on characterizing the surface marker expression of the immortalized LCLs. This study demonstrates the generation of 15 LCLs from sixteen rheumatoid arthritis (RA) patients and a healthy volunteer using B95-8 marmoset-derived EBV. The success rate of LCL generation was 88.23%. All CD19+ LCLs expressed CD23 (16.94-58.9%) and CD27 (15.74-80.89%) on cell surface. Our data demonstrated two distinct categories of LCLs (fast- and slow-growing) (p<0.05) based on their doubling time. The slow-growing LCLs showed lower CD23 level (35.28%) compared to fast-growing LCLs (42.39%). In contrast, the slow-growing LCLs showed higher percentage in both CD27 alone and CD23+CD27+ in combination. Overall, these findings may suggest the correlations of cellular CD23 and CD27 expression with the proliferation rate of the generated LCLs. Increase expression of CD23 may play a role in EBV immortalization of B-cells and the growth and maintenance of the EBV-transformed LCLs while CD27 expression might have inhibitory effects on LCL proliferation. Further investigations are warranted to these speculations.
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Hibbert, Richard G., Peter Teriete, Gabrielle J. Grundy, Rebecca L. Beavil, Rajko Reljić, V. Michael Holers, Jonathan P. Hannan, Brian J. Sutton, Hannah J. Gould, and James M. McDonnell. "The structure of human CD23 and its interactions with IgE and CD21." Journal of Experimental Medicine 202, no. 6 (September 19, 2005): 751–60. http://dx.doi.org/10.1084/jem.20050811.
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The low-affinity immunoglobulin E (IgE) receptor, CD23 (FcεRII), binds both IgE and CD21 and, through these interactions, regulates the synthesis of IgE, the antibody isotype that mediates the allergic response. We have determined the three-dimensional structure of the C-type lectin domain of CD23 in solution by nuclear magnetic resonance spectroscopy. An analysis of concentration-dependent chemical shift perturbations have allowed us to identify the residues engaged in self-association to the trimeric state, whereas ligand-induced changes have defined the binding sites for IgE and CD21. The results further reveal that CD23 can bind both ligands simultaneously. Despite the C-type lectin domain structure, none of the interactions require calcium. We also find that IgE and CD23 can interact to form high molecular mass multimeric complexes. The interactions that we have described provide a solution to the paradox that CD23 is involved in both up- and down-regulation of IgE and provide a structural basis for the development of inhibitors of allergic disease.
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Dorion, R. Patrick, and John H. Shaw. "Intracytoplasmic Filamentous Inclusions in the Peripheral Blood of a Patient With Chronic Lymphocytic Leukemia." Archives of Pathology & Laboratory Medicine 127, no. 5 (May 1, 2003): 618–20. http://dx.doi.org/10.5858/2003-127-0618-ifiitp.
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Abstract Intracellular inclusions in lymphoproliferative disorders are not common. Multiple different types of inclusions have been reported in chronic lymphocytic leukemia (CLL), including vacuoles, crystals, and pseudocrystals. Most of the reported cases were seen in the bone marrow lymphocytes, and the majority of these on electron microscopy. We report a case of long-standing CLL with no therapy that had filamentous cytoplasmic inclusions in the peripheral blood that were readily seen by light microscopy. Electron microscopy demonstrated dilated cisternae of the rough endoplasmic reticulum filled with amorphous electron-dense material. By immunofluorescence, the material proved to be immunoglobulin G-λ deposits. The immunophenotype had the typical CLL pattern with positive staining with CD19, CD5, and CD23, and low-density CD20 staining; however, it also had unusual staining with CD25 and intermediate-intensity staining with CD22.
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Otsuka, Masaki, Yoshihiro Yakushijin, Makoto Hamada, Takaaki Hato, Masaki Yasukawa, and Sigeru Fujita. "The Expression of the CD21 Antigen in Non-Hodgkin’s Lymphoma Is Involved in LFA-1 Expression and Tumor Survival." Blood 104, no. 11 (November 16, 2004): 2285. http://dx.doi.org/10.1182/blood.v104.11.2285.2285.
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Abstract CD21/complement receptor type 2 is a membrane protein expressed on B lymphocytes, follicular dendritic cells, early thymocytes, and a subset of mature T lymphocytes. This major B cell antigen appears later than CD19 and CD20 in cell differentiation and is lost from the cell surface during the early stages of B cell activation. CD21 is characterized not only as a complement ligand but also as an adhesion molecule of the cell surface that is dependent on CD23 expression, suggesting that it may be involved in lymphocyte trafficking and several immune responses. Recently two groups have reported that CD21 expression is significantly negatively associated with mortality in diffuse large B cell lymphomas. From these reports and clinical observations, we have transfected the CD21 gene into a CD21/CD23-negative lymphoma cell line (Namalwa). Interestingly, all established CD21+ transfectants (six clones from different bulks) showed homotypic aggregation during in vitro cell culturing, and none of the anti-CD21 antibodies prevented this cell aggregation. Moreover, these CD21+ transfectants were easily rejected in vivo when they were injected in nude mice compared to vector-only transfectants and parental cells as controls. These observations suggest that other adhesion molecules may be involved in CD21-induced cell aggregation and reduced tumorgenesis in vivo. After the screening of several integrins, CD21+ transfectants highly expressed LFA-1 (CD11a/CD18) on their cell surfaces compared to vector-only transfectants and parental cells. CD21+ transfectants displayed tight adhesion when in contact with recombinant human ICAM-1, and cell aggregation of CD21+ transfectants was blocked by an anti-LFA-1 monoclonal antibody. Northern and Western analysis and confocal laser scanning microscopic analysis suggested that the CD21 expression made the transfer of LFA-1 from the cytoplasm to the cell surface. We conclude that the expression of the CD21 molecule is strongly associated with the LFA-1 expression on the cell surface, independent of the CD23 molecule, and this phenomenon may be involved in tumor survival in non-Hodgkin’s lymphoma in vivo.
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Giordano Attianese, Greta Maria Paola, Virna Marin, Valentina Hoyos, Barbara Savoldo, Irene Pizzitola, Sarah Tettamanti, Valentina Agostoni, et al. "In vitro and in vivo model of a novel immunotherapy approach for chronic lymphocytic leukemia by anti-CD23 chimeric antigen receptor." Blood 117, no. 18 (May 5, 2011): 4736–45. http://dx.doi.org/10.1182/blood-2010-10-311845.
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Abstract Chronic lymphocytic leukemia (CLL) is characterized by an accumulation of mature CD19+CD5+CD20dim B lymphocytes that typically express the B-cell activation marker CD23. In the present study, we cloned and expressed in T lymphocytes a novel chimeric antigen receptor (CAR) targeting the CD23 antigen (CD23.CAR). CD23.CAR+ T cells showed specific cytotoxic activity against CD23+ tumor cell lines (average lysis 42%) and primary CD23+ CLL cells (average lysis 58%). This effect was obtained without significant toxicity against normal B lymphocytes, in contrast to CARs targeting CD19 or CD20 antigens, which are also expressed physiologically by normal B lymphocytes. Moreover, CLL-derived CD23.CAR+ T cells released inflammatory cytokines (1445-fold more TNF-β, 20-fold more TNF-α, and 4-fold more IFN-γ). IL-2 was also produced (average release 2681 pg/mL) and sustained the antigen-dependent proliferation of CD23.CAR+ T cells. Redirected T cells were also effective in vivo in a CLL Rag2−/−γc−/− xenograft mouse model. Compared with mice treated with control T cells, the infusion of CD23.CAR+ T cells resulted in a significant delay in the growth of the MEC-1 CLL cell line. These data suggest that CD23.CAR+ T cells represent a selective immunotherapy for the elimination of CD23+ leukemic cells in patients with CLL.
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Lee, Hye Won, Hyunwoo Lee, Chanho Park, Won Joon Oh, Tae Jin Kim, Ghee Young Kwon, and Seong Il Seo. "Pattern of Tumor-Infiltrating Lymphocytes in Mixed Epithelial and Stromal Tumor of the Kidney: A Review of Five Cases." Cells 10, no. 4 (April 16, 2021): 917. http://dx.doi.org/10.3390/cells10040917.
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Mixed epithelial and stromal tumor of the kidney (MESTK), a benign rare tumor with malignant transformation potential, is thought to be derived from fetal or immature cells originating from the mesonephric and Müllerian ducts. However, due to its rarity, little is known about the anti-tumor immune responses in MESTK. Herein, we present five cases of MESTK and evaluate the population of tumor-infiltrating lymphocytes (TILs) using a freshly obtained MESTK sample. Microscopically, TILs were scattered or clustered in large aggregates in the stroma in all five cases; furthermore, three cases exhibited heavy, large lymphocytic aggregates with no well-organized tertiary lymphoid structures with germinal centers. Flow cytometric analysis of TILs in one freshly obtained MESTK sample revealed that >40% of CD3+ T cells were effector memory Fas+CD28− γδ T cells expressing high levels of programmed cell death protein 1 and inducible T-cell co-stimulator, but low levels of CD44 and CD27. Most αß T cells exhibited a naïve phenotype. Additionally, we detected many activated class-switched CD21+CD27+ B cells as well as CD11chighIgMhigh marginal zone B-like and CD27−CD21−CD23− immunoglobulin (Ig)DhighIgMlow age-associated B-like cells. Collectively, for the first time, we report the immune microenvironment pattern of MESTK to oncogenic stress.
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Onguru, Daniel, YanMei Liang, Jennifer Elliot, Pauline Mwinzi, and Lisa Ganley-Leal. "CD23b Isoform Expression in Human Schistosomiasis Identifies a Novel Subset of Activated B Cells." Infection and Immunity 79, no. 9 (June 27, 2011): 3770–77. http://dx.doi.org/10.1128/iai.05094-11.
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ABSTRACTResistance to schistosomiasis is associated with increased levels of serum parasite-specific IgE. IgE exerts its functions through its cellular receptors, FcεRI and FcεRII/CD23; however, its functional significance in humans requires further characterization. We previously reported that increased levels of CD23+B cells correlate with resistance to schistosomiasis in hyperexposed populations and sought to define their potential function and relationship with IgE. We found that CD23+B cells are a heterogeneous cell population with functional and phenotypic differences. Circulating CD23+B cells are uniquely activated in schistosomiasis and express the CD23b isoform and CXCR5, the homing receptor for lymphoid follicles. High CXCR5 expression by CD23+B cells was associated with the capacity to home to the cognate ligand CXCL13. CD23-bound IgE cross-linking increased surface expression of CXCR5, suggesting that CD23+B cells home directly into the lymphoid follicles upon antigen capture. As human schistosomiasis is an intravascular parasitic infection associated with a high antigenic burden in the blood, circulating CD23+B cells may play a role in the capture and shuttling of antigens directly to splenic follicles, highlighting a new role for circulating B cells. This function likely plays an important role in the development of protective immunity to infection with schistosomes.
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Semanaj, Valentina, Arbi Pecani, Teuta Dedej, Alma Barbullushi, Zamira Ylli, Teuta Curaj, Polikron Pulluqi, et al. "The Diagnostic Value of Flow Cytometry Imunophenotyping in an Albanian Patient Population with a Preliminary Clinical Diagnosis of Chronic Lymphocytic Leukemia." Open Access Macedonian Journal of Medical Sciences 2, no. 1 (March 15, 2014): 51–55. http://dx.doi.org/10.3889/oamjms.2014.009.
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Objective: Based on the flow cytometry multiparametric immunophenotyping methodology we studied some useful cell marker criteria needed for the practical differentiation of the chronic lymphocytic leukemia from other chronic limphoproliferative diseases with a leukemic component.Materials and Methods: The applied methodology is a four color flow cytometry multiparametric immunophenotyping technique using EDTA blood samples taken from 84 consecutive patients diagnosed with CLL through a preliminary clinical and white blood cell examination. The following fluorescent stained monoclonal antibodies were used: CD3, CD4, CD5, CD8, CD11c, CD19, CD20, CD23, CD25, FMC7 and kappa/lambda light chains.Results: From the 84 individuals tested, 2 out of them (2.4%) resulted with a abnormal T-cell population while 82 (97.6%) showed a pathological B cell line. 58 (69.1%) patients resulted with typical CLL markers (CD19+CD5+CD23+) while 5 (5.9%) of them presented a non typical chronic lymphocytic leukemia profile (CD19+CD5+CD23-). 19 (22.6%) out of patients displayed an abnormal CD19+CD5- B cell population. A statistically significant correlation was found between the clinical stage of CLL and the positivity for the CD38 marker (p=0.04).Conclusion: Flow cytometry immunophenotyping is a fundamental examination for the final diagnosis of chronic lymphocytic leukemia. The expression of CD38+ in CLL patients stands for a more advanced clinical stage.
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Gu, B., L. J. Bendall, and J. S. Wiley. "Adenosine Triphosphate–Induced Shedding of CD23 and L-Selectin (CD62L) From Lymphocytes Is Mediated by the Same Receptor but Different Metalloproteases." Blood 92, no. 3 (August 1, 1998): 946–51. http://dx.doi.org/10.1182/blood.v92.3.946.
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Abstract CD23 is a transmembrane protein expressed on the surface of B-lymphocytes that binds IgE, CD21, CD11b, and CD11c. High concentrations of soluble CD23 and L-selectin are found in the serum of patients with B-chronic lymphocytic leukemia (B-CLL). Because extracellular adenosine triphosphate (ATP) causes shedding of L-selectin via activation of P2Z/P2X7 receptors expressed on B-CLL lymphocytes, we studied the effect of ATP on shedding of CD23. ATP-induced shedding of CD23 at an initial rate of 12% of that for L-selectin, whereas the EC50 for ATP was identical (35 μmol/L) for shedding of both molecules. Furthermore, benzoylbenzoyl ATP also produced shedding of CD23 and L-selectin with the same agonist EC50 values for both (10 μmol/L). Inactivation of the P2Z/P2X7 receptor by preincubation with oxidized ATP abolished ATP-induced shedding of both molecules. Moreover, KN-62, the most potent inhibitor for the P2Z/P2X7 receptor, inhibited ATP-induced shedding of both CD23 and L-selectin with the same IC50 (12 nmol/L). Ro 31-9790, a membrane permeant zinc chelator that inhibits the phorbol-ester-stimulated shedding of L-selectin, also inhibited shedding of CD23 from B-CLL lymphocytes. However, the IC50 for this inhibition by Ro31-9790 was different for L-selectin and CD23 (83 v 6 μmol/L, respectively). Although L-selectin was completely shed by incubation of cells with phorbol-ester, CD23 was not lost under these conditions. The data show that extracellular ATP induces shedding of L-selectin and CD23 from B-CLL lymphocytes by an action mediated by the P2Z/P2X7 receptor. However, different membrane metalloproteases seem to mediate the shedding of L-selectin and CD23. © 1998 by The American Society of Hematology.
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Gu, B., L. J. Bendall, and J. S. Wiley. "Adenosine Triphosphate–Induced Shedding of CD23 and L-Selectin (CD62L) From Lymphocytes Is Mediated by the Same Receptor but Different Metalloproteases." Blood 92, no. 3 (August 1, 1998): 946–51. http://dx.doi.org/10.1182/blood.v92.3.946.415a24_946_951.
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CD23 is a transmembrane protein expressed on the surface of B-lymphocytes that binds IgE, CD21, CD11b, and CD11c. High concentrations of soluble CD23 and L-selectin are found in the serum of patients with B-chronic lymphocytic leukemia (B-CLL). Because extracellular adenosine triphosphate (ATP) causes shedding of L-selectin via activation of P2Z/P2X7 receptors expressed on B-CLL lymphocytes, we studied the effect of ATP on shedding of CD23. ATP-induced shedding of CD23 at an initial rate of 12% of that for L-selectin, whereas the EC50 for ATP was identical (35 μmol/L) for shedding of both molecules. Furthermore, benzoylbenzoyl ATP also produced shedding of CD23 and L-selectin with the same agonist EC50 values for both (10 μmol/L). Inactivation of the P2Z/P2X7 receptor by preincubation with oxidized ATP abolished ATP-induced shedding of both molecules. Moreover, KN-62, the most potent inhibitor for the P2Z/P2X7 receptor, inhibited ATP-induced shedding of both CD23 and L-selectin with the same IC50 (12 nmol/L). Ro 31-9790, a membrane permeant zinc chelator that inhibits the phorbol-ester-stimulated shedding of L-selectin, also inhibited shedding of CD23 from B-CLL lymphocytes. However, the IC50 for this inhibition by Ro31-9790 was different for L-selectin and CD23 (83 v 6 μmol/L, respectively). Although L-selectin was completely shed by incubation of cells with phorbol-ester, CD23 was not lost under these conditions. The data show that extracellular ATP induces shedding of L-selectin and CD23 from B-CLL lymphocytes by an action mediated by the P2Z/P2X7 receptor. However, different membrane metalloproteases seem to mediate the shedding of L-selectin and CD23. © 1998 by The American Society of Hematology.
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Dragovic-Ivancevic, Tijana, Nada Kraguljac-Kurtovic, Vesna Knezevic, Andrija Bogdanovic, Biljana Mihaljevic, Biljana Bozic, and Mirjana Gotic. "The role of immunophenotyping in differential diagnosis of chronic lymphocytic leukemia." Srpski arhiv za celokupno lekarstvo 142, no. 3-4 (2014): 197–203. http://dx.doi.org/10.2298/sarh1404197d.
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Introduction. Accurate diagnosis of chronic lymphocytic leukemia (CLL) acquires immunophenotyping by flow cytometry in order to facilitate differential diagnosis between CLL and other mature B-cell neoplasms (MBCN). Objective. The aim of this study was to define immunological profile of CLL cells. Methods. Immunophenotyping by flow cytometry was performed on peripheral blood specimens at diagnosis in the group of 211 patients with de novo MBCN. Results. Absolute count of B-cells was significantly increased in all MBCN patients comparing to healthy control group (p<0.05). B-cell monoclonality was detected in 96% of all MBCN patients, by using surface immunoglobulin (sIg) light chain restriction. B-cell antigens, CD19, CD20, CD22, were expressed with very high frequency in CLL and other MBCN. In comparison with other MBCN, in CLL group, the frequency of expression was higher for CD5 and CD23 (p<0.0001), though lower for FMC7 antigen (p<0.0001). CLL patients were characterized by lower expression patterns of CD20, CD22, CD79b, and sIg (p<0.0001) as well as higher expression pattern of CD5 antigen (p<0.05). Correlation between the final diagnosis of MBCN and values of CLL scoring system showed that the majority of CLL patients (97%) had higher values (5 or 4) whereas the majority of other MBCN patients (96%) had lower score values (0-3). Conclusion. Our results have shown that characteristic immunophenotype which differentiates CLL from other MBCN is defined by following marker combination - CD19+ CD20+low CD22+low CD5+high CD23+ FMC7- CD79b+low sIg+low. CLL score values of 5 or 4 points are highly suggestive for diagnosis of CLL.
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Bonnefoy, Jean-Yves, Jean-François Gauchat, Paul Life, Pierre Graber, Jean-Pierre Aubry, and Sybille Lecoanet-Henchoz. "Regulation of IgE Synthesis by CD23/CD21 Interaction." International Archives of Allergy and Immunology 107, no. 1-3 (1995): 40–42. http://dx.doi.org/10.1159/000236924.
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Attianese, Greta Maria Paola Giordano, Valentina Hoyos, Virna Marin, Barbara Savoldo, Irene Pizzitola, Valentina Agostoni, Matteo Parma, et al. "A New Chimeric Antigen Receptor (CAR) Targeting the CD23 Antigen Expressed by Chronic Lymphocytic Leukemia (B-CLL) Cells." Blood 116, no. 21 (November 19, 2010): 2446. http://dx.doi.org/10.1182/blood.v116.21.2446.2446.
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Abstract Abstract 2446 B-Chronic lymphocytic leukemia (B-CLL) is characterized by a progressive accumulation of B-lymphocytes expressing CD19, CD20dim and aberrantly expressing the CD5 T-cell marker. Moreover, they over-express the B-cell activation marker CD23. Chimeric Antigen Receptors (CAR) are engineered molecules able to redirect T-cell killing/effector activity towards a selected target in a non MHC-restricted manner. First trials targeting B-CLL were based on both monoclonal antibodies and anti-CD19/anti-CD20.CAR-transduced T cells. However, this approach causes the elimination of normal B-lymphocytes and B-precursors with consequent impairment of humoral immunity. Selective CD23 expression on B-CLL cells renders this molecule an optimal target to design a specific CAR. We have generated a novel CD23-targeting CAR to redirect T cells against CD23+B-CLL. Transduced T cells were tested for cytotoxicity against different CD23+-targets, using a classic 51Chromium release assay, and for specific cytokine release, by multiplex flow cytomix assay. T cells from B-CLL patients were efficiently transduced with the anti-CD23.CAR (average expression 68%, n=10) and redirected specifically toward autologous blasts (average lysis 58%, n=5). On the contrary, anti-CD23 transduced T-cells did not displayed any relevant killing versus normal B cells (average lysis 13%, n=3), differently from anti-CD19.CAR redirected T-cells, which killed tumor and normal B cells in an indistinct manner. Moreover, anti-CD23.CAR redirected T lymphocytes derived from both healthy donors (HD) and B-CLL patients displayed a specific lytic activity against CD23+EBV-LCLs, even in presence of soluble CD23 enriched plasma without being inhibited (average lysis with no plasma 67%; average lysis with 25% of CD23 enriched plasma 79%; average lysis with 50% of CD23 enriched plasma 88%, n=3). We also demonstrated that the expression of the anti-CD23.CAR caused a significant increase in cytokine release from transduced in vitro activated T cells after a 48h stimulation with CD23+ targets. B-CLL derived CD23.CAR-expressing T cells (n=3) secreted 4-fold more INF-gamma, and 1445-fold more TNF-beta, compared to non transduced T cells. Interleukin-2 was also released (average release 2681 pg/mL, n=3) and sustained the antigen-dependent proliferation of CD23.CAR+T cells. To confirm in vivo the in vitro data, we tested NT and CD23.CAR transduced T cells in a recently published xenograft model of B-CLL (Ref biblio, primo nome, giornale, anno). This model is based on the intravenous or subcutaneous injection of the established human B-CLL cell line MEC1 into Rag2−/− gammac−/− mice, which lack not only B and T cells, but also natural killer (NK) cells, thus presenting a profound immunosuppressive environment leading to an high efficiency of both B-CLL and T-cell engraftment. Moreover, this model reproduces the systemic involvement of the disease and it closely resembles the aggressive form human B-CLL, representing an optimal experimental setting to test the efficacy of new therapeutic agents. In the first set of our experiments, 8 weeks-old male mice were subcutaneously injected with 10*106 MEC1 cells in the left flank. Then, mice bearing an established tumor were treated intravenously with a single dose of NT or engineered CD23.CAR T cells (2*106), without any addition of exogenous IL-2. Animals were monitored twice a week for weight and tumor growth (measuring three perpendicular diameters), and sacrificed when the mean tumor volume reached a dimension of 31000 mm3, before presenting clinical signs and symptoms. Compared with NT-treated mice, the infusion of CD23.CAR+T cells resulted in a significant delay in tumor growth, as measured by tumor volume diameter/day (CD23.CAR+ T cells vs NT T cells: p=0.04 at day 12; n=3). In conclusion, our results suggest that CD23.CAR-redirected T cells provide cytotoxic activity against CD23+ B-CLL cells in vitro and in vivo, while sparing normal B lymphocytes, as compared to other available CARs targeting pan-B-cell antigens, such as CD19 and CD20. These results are encouraging and demonstrate the feasibility of generating CD23.CAR+ T lymphocytes for adoptive T-cell therapy of patients with B-CLL. Disclosures: No relevant conflicts of interest to declare.
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Huang, N., MM Kawano, MS Mahmoud, K. Mihara, T. Tsujimoto, O. Niwa, and A. Kuramoto. "Expression of CD21 antigen on myeloma cells and its involvement in their adhesion to bone marrow stromal cells." Blood 85, no. 12 (June 15, 1995): 3704–12. http://dx.doi.org/10.1182/blood.v85.12.3704.bloodjournal85123704.
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The mature myeloma cells express very late antigen 5 (VLA-5) and MPC-1 antigens on their surface and adhere to bone marrow (BM) stromal cells more tightly than the VLA-5-MPC-1-immature myeloma cells in vitro. The VLA-5 and MPC-1 antigens possibly function as two of the molecules responsible for interaction of mature myeloma cells with BM stromal cells. However, the immature myeloma cells do interact with BM stromal cells, and it is unclear which adhesion molecules mediate their interaction. In this study, we found that both immature and mature myeloma cells expressed CD21, an adhesion molecule known to bind to CD23. CD21 was also detected on normal plasma cells. To evaluate the role of CD21 expression on myeloma cells, two myeloma cell lines, NOP-2 (VLA-5-MPC-1-) and KMS-5 (VLA-5+MPC-1+), were used as representatives of immature and mature myeloma cell types, respectively, and an adhesion assay was performed between the myeloma cell lines and BM stromal cells. Antibody-blocking results showed that adhesion of the mature type KMS-5 to KM102, a human BM-derived stromal cell line, or to short-term cultured BM primary stromal cells was inhibited by monoclonal antibodies (MoAbs) against CD21, VLA-5, and MPC-1, and inhibition of adhesion of the immature type NOP-2 to KM102 by the anti-CD21 MoAb was observed as well. Furthermore, CD23 was detected on KM102. Treatment of KM102 with an anti-CD23 MoAb also inhibited adhesion of either KMS-5 or NOP-2 to KM102. Therefore, we propose that CD21 expressed on myeloma cells likely functions as a molecule responsible for the interaction of immature myeloma cells as well as mature myeloma cells with BM stromal cells, and CD23 may be the ligand on the stromal cells for the CD21-mediated adhesion.
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Rosenwasser, Lanny J., and Jianfeng Meng. "Anti-CD23." Clinical Reviews in Allergy & Immunology 29, no. 1 (2005): 061–72. http://dx.doi.org/10.1385/criai:29:1:061.
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Zhang, John, David Chin, Adam Anthony, Heather Bolton, Cheri Phillips, Anselm Hii, and Sing-Tsung Chen. "CD5 and CD23 Positive Mantle Cell Lymphoma Detected by Flow Cytometry and Confirmed by FISH Study t(11;14)." Blood 104, no. 11 (November 16, 2004): 4814. http://dx.doi.org/10.1182/blood.v104.11.4814.4814.
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Abstract The differential diagnoses of CD5 positive B-cell lymphoproliferative disorders mainly include chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) and mantle cell lymphoma. Occasionally large cell and marginal zone lymphomas may also be CD5 positive. An accurate diagnosis effects patient management. The classical immunophenotype for chronic lymphocytic leukemia/small lymphocytic lymphoma is CD19/CD5/CD23 positive FMC-7 negative cells with dim CD20 and dim light chain expressions, while mantle cell lymphoma is CD19/CD5/FMC-7 positive with bright CD20 and bright light chain expressions. The diagnosis of mantle cell lymphoma is usually confirmed by either immunostain for cyclin D1 or FISH study for t(11;14). In reality, immunostaining for cyclin D1 can be difficult and may show variable results in different laboratories and FISH study may not be readily available. Generally, when it comes to the diagnosis of lymphoma, immunohistochemical positivity of both CD5 and CD23 is almost pathognomic for chronic lymphocytic leukemia/small lymphocytic lymphoma if no fresh tissue is saved for flow cytometry analysis. Flow cytometry analysis of 44 FISH-confirmed mantle cell lymphomas was reviewed in our lab. Among these, 37 showed the classical immunophenotype of mantle cell lymphoma. However, 7 cases (16%) were positive for both CD5 and CD23. The expression of CD23 varied from dim to bright. When compared to typical CLL, they showed FMC-7 expression and brighter than dim light chain expression. In one case, the light chain expression was dim. In conclusion, CD23 expression which was thought to be a specific marker for CLL/SLL may also be seen with mantle cell lymphoma. Although FMC-7 expression is seen in all CD23 positive mantle cell lymphomas, bright light chain expression is not universal. We recommend that FISH or immunohistochemical studies for cyclin D1 be performed on CD5/CD19 clonal B cell proliferations with CD23 expression if morphology or immunophenotype is atypical for CLL/SLL.
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Kusakabe, Manabu, Guillermo Simkin, Justin Meskas, Chaoran Zhang, Daisuke Ennishi, Merrill Boyle, David W. Scott, et al. "Single Cell Mass Cytometry for Phenotypic Analysis of Diffuse Large B-Cell Lymphoma." Blood 124, no. 21 (December 6, 2014): 2976. http://dx.doi.org/10.1182/blood.v124.21.2976.2976.
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Abstract Diffuse Large B-cell Lymphoma (DLBCL) is the most common histologic subtype of non-Hodgkin Lymphoma (NHL). Despite its improved outcome with R-CHOP chemotherapy, 40% of patients still suffer with relapsed or refractory disease. Further investigation is needed to understand the complexity of DLBCL. Time-of-flight mass cytometry (CyTOF) is a recently developed technology that combines traditional flow cytometry with mass spectrometry and supports analysis of up to 30-40 parameters simultaneously at the single cell level with minimal spectral overlap (Bendall et al, Science 2011). In this study, we sought to develop a CyTOF method for phenotypic analysis of DLBCL to obtain high resolution profiles of the malignant clone(s) represented in individual tumor samples and resolve any underlying population substructure that might be informative in understanding the clinical and biologic heterogeneity of this disease. We designed a two-tube assay for this study. Tube #1 contained 35 cell surface markers including CD45, CD19, CD20, CD22, CD79B, IgM, IgD, Ig Kappa, Ig Lambda, CD5, CD10, CD23, CD43, CD38, CD138, CD44, CD21, CD24, CD40, CD72, CD80, CD45RA, CD49D, CD49F, CD62L, CD25, CD27, CD30, CD127, CD184, CD194, CD200, CD34, HLA-DR, and CD3. Tube #2 contained 37 markers in total including 17 cell surface markers overlapping with Tube #1 plus an additional 20 intracellular markers (BCL2, BCL6, IRF4/MUM1, LMO2, MYC, MCL1, MEF2B, KAT3B/P300, CBP, FOXP1, RUNX1, Ikaros, EZH2, BMI1, NOTCH1, CARD11, IkBa, phospho-Rb, Ki67, and CyclinD2). Metal-conjugated antibodies were purchased from DVS Sciences or unconjugated antibodies labeled in-house using DVS MaxPar metal labeling kits. Data were acquired using a DVS CyTOF2 instrument. We examined both fresh and viably frozen single cell suspensions from diagnostic lymph node biopsy samples received for flow cytometric analysis at the BC Cancer Agency. We used SPADE (spanning-tree progression analysis of density-normalized events) for initial data analysis. We first performed preliminary validation studies including cross-comparison of mass cytometry (CyTOF2) vs. flow cytometry (BD Canto2) datasets and fresh vs. previously frozen cell suspension material. Although individual marker intensities using matched antibody clones were in general lower by CyTOF, eight-parameter surface staining results were qualitatively comparable between the two platforms. Also there were essentially no differences observed in CyTOF staining profiles between fresh and previously frozen samples. Preliminary clustering analysis of cell populations using SPADE revealed clear separation between normal and malignant B cell populations as well as apparent substructure to the malignant population in a subset of DLBCL samples. These findings suggest intratumoral heterogeneity can be resolved by high dimensional CyTOF analysis. Ongoing efforts will focus on determining if phenotypically defined subsets show enrichment for subclonal mutations. Disclosures No relevant conflicts of interest to declare.
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Armas-González, Estefanía, Ana Díaz-Martín, María Jesús Domínguez-Luis, María Teresa Arce-Franco, Ada Herrera-García, María Vanesa Hernández-Hernández, Sagrario Bustabad, et al. "Differential Antigen-presenting B Cell Phenotypes from Synovial Microenvironment of Patients with Rheumatoid and Psoriatic Arthritis." Journal of Rheumatology 42, no. 10 (July 15, 2015): 1825–34. http://dx.doi.org/10.3899/jrheum.141577.
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Objective.To study the qualitative and quantitative phenotypic changes that occur in molecules involved in antigen presentation and costimulation in synovial B cells from rheumatoid arthritis (RA) and psoriatic arthritis (PsA).Methods.The presence of HLA-DR, CD86, and CD40 in CD20+ cells was studied in RA synovium biopsies using immunohistochemistry and immunofluorescence. Expression was assessed by flow cytometry of the Class II molecules CD40, CD86, CD23, and CD27 on B cells from the synovial fluid (SF), with respect to peripheral blood, from 13 patients with RA and 15 patients with PsA. Expression of interferon-induced protein with tetratricopeptide repeats 4 (IFIT4) in immune-selected CD20+ cells from patients with RA was assessed by quantitative realtime PCR.Results.Infiltrating synovial RA, B cells expressed HLA-DR, CD40, and CD86. Increased expression of CD86, HLA-DR, and HLA-DQ in B cells from SF was found in patients with RA and PsA. HLA-DP was also elevated in rheumatoid SF B cells; conversely, a significantly lower expression was observed in SF from patients with PsA. CD40 expression was increased in SF B cells from PsA, but not in patients with RA. Interestingly, CD20 surface expression level was significantly lower in SF B cells (CD19+, CD138−) from RA, but not in patients with PsA. CD27 upregulation and CD23 downregulation were observed in synovial B cells in both pathologies. Finally, a 4-fold increase in IFIT4 mRNA content was shown in B cells from SF in patients with RA.Conclusion.Synovial B cells from patients with RA and patients with PsA express different antigen-presenting cell phenotypes, suggesting that this cell type plays a dissimilar role in the pathogenesis of each disease.
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Waller, EK, M. Ziemianska, CD Bangs, M. Cleary, I. Weissman, and OW Kamel. "Characterization of posttransplant lymphomas that express T-cell- associated markers: immunophenotypes, molecular genetics, cytogenetics, and heterotransplantation in severe combined immunodeficient mice." Blood 82, no. 1 (July 1, 1993): 247–61. http://dx.doi.org/10.1182/blood.v82.1.247.bloodjournal821247.
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Immunosuppressed individuals are at high risk for the development of hematologic malignancies. The typical lymphomas arising in organ transplant recipients are B-cell non-Hodgkin's lymphomas that contain Epstein-Barr virus (EBV) DNA sequences. We investigated the characteristics of posttransplant lymphomas that lacked expression of the usual markers associated with EBV transformation. We describe four large-cell lymphomas seen recently at our institution. Two of these four cases were CD4+, one was CD8+, and in one staining for CD4 and CD8 expression was not performed. One CD4+ lymphoma was a CD30+, EBV- large- cell lymphoma from a 65-year-old kidney transplant recipient, the second was an EBV+ large-cell lymphoma from a 25-year-old heart transplant patient. Two T-cell lymphomas were EBV+ and had clonal T- cell receptor beta gene rearrangements. The other two lymphomas expressed T-cell markers CD4 and CD43, and lacked expression of B-cell markers CD19, CD20, CD21, CD22, CD23, and surface Ig. Both CD4+ lymphomas were tumorigenic after their heterotransplantation into severe combined immunodeficient (SCID) mice. Cytogenetics, immunophenotyping, and genotyping of the secondary tumors from SCID mice showed their clonality and identity with the patients' primary tumors. Novel CD4+ lymphoma cell lines, LH521/4 and LK418/4, were established from tumors that had been passaged in SCID mice. An immunodeficient environment may facilitate the growth of these T-cell or biphenotypic lymphomas; the etiology of their genesis can include transformation with EBV and other, as yet unidentified mechanisms.
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Rozana, Nazaryan, Kryvenko Liudmyla, and Gargin Vitaliy. "Peculiarities of vascular endothelial growth factor of oral cavity in atopic condition VEGF of oral cavity in atopic condition." Interventional Medicine and Applied Science 11, no. 4 (August 5, 2021): 207–12. http://dx.doi.org/10.1556/1646.2020.00002.
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AbstractBackground and aimsVascular endothelial growth factor (VEGF) is regarded as a potent stimulating factor for angiogenesis and vascular permeability and probably is connected with an inflammatory reaction. Our study aimed to determine the effect of VEGF in the inflammatory process in the oral mucosa of experimental animals in the modulation of atopic disease.Materials and methodsAtopic condition was simulated by the ovalbumin model. Obtained specimens of oral mucosa were examined histologically; immunohistochemistry was performed with detection VEGF, CD23, CD20.ResultsMost pronounced changes with twice increased expression activity of VEGF has been detected in the affected areas of the lamina propria and were associated with perivascular inflammatory microinfiltration, but unexpected expression in the epithelial layer has been revealed surround of intraepithelial inflammatory cells mainly. Pronounced correlations have been detected as VEGF and CD23 (r = 0.91), VEGF and CD20 (r = 0.87), CD23 and CD20 (r = 0.89).Discussiondescribed the changes in the tissues of the oral mucosa could be served as a basis for the development of preventive measures in patients with atopic diseases.discussionConclusionsActivation of VEGF is connected with accumulation of inflammatory infiltrate represented by B-lymphocytes, activated macrophages, eosinophils with a correlation in atopic process.
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Thornton, Catherine A., Judith A. Holloway, and John O. Warner. "Expression of CD21 and CD23 during Human Fetal Development." Pediatric Research 52, no. 2 (August 2002): 245–50. http://dx.doi.org/10.1203/00006450-200208000-00017.
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Marsilio, Sonia, Barbara Sherry, Xiao J. Yan, Jacqueline C. Barrientos, Steven L. Allen, Jonathan E. Kolitz, Kanti R. Rai, and Nicholas Chiorazzi. "CLL Sera Drive Maturation of Normal Monocytes to M2-like Macrophages By Direct and Indirect Mechanisms." Blood 124, no. 21 (December 6, 2014): 1970. http://dx.doi.org/10.1182/blood.v124.21.1970.1970.
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Abstract Background. Chronic lymphocytic leukemia (CLL) is a prototypic microenvironment-dependent B-cell malignancy, in which neoplastic B cells co-evolve with a supportive tissue microenvironment to promote leukemia cell survival, growth, and drug-resistance. Within the microenvironment, hematopoietic and non-hematopoietic stromal and tumor cells produce factors that recruit circulating monocytes to tumor sites and induce differentiation into macrophages. Mirroring the Th1/Th2 paradigm, cells of monocyte-macrophage lineage reprogram their functions in response to environmental signals, undergoing M1 (classical) or M2 (alternative) activation, which represent extremes of a broad continuum of functional states. Classical M1 cells (activated by IFNs and TLR) are involved as inducer and effectors cells in polarized Th1 responses and as effectors of resistance against intracellular parasites and tumors. In contrast, M2 cells (activated by IL4 and IL13) are poor at antigen presentation, suppress Th1 adaptive immunity, actively scavenge debris, contribute to the dampening of inflammation, promote angiogenesis and tissue remodeling, and support tumor progression. One way to distinguish the two types of macrophages is based on surface antigen expression: M1-like cells up-regulate Fcg receptors I, II, III such as CD16, CD32 and CD64, whereas M2-like macrophages display abundant levels of CD23, CD163, and scavenger receptors (e.g. MCR1). Understanding the microenvironment and the crosstalk between B-CLL cells and their tissue neighbors can give insight into disease biology and for therapy. Aim. To investigate if the CLL milieu, contained within serum, influences monocyte-to-macrophage differentiation, promoting an anti (M2)- or pro (M1)- inflammatory microenvironment. Methods. Monocytes from healthy donors were isolated using Monocytes Isolation Kit II (Miltenyi) and cultured in Ultra-Low Attachment plates with 10% normal human AB serum or 10% CLL-derived serum -/+ IL4 or IFNg for 3 days. Macrophages were stained for CD23, CD64, CD32, MRC1, CD14, CD16, and data were acquired with a BD LSRII flow cytometer and analyzed by FlowJo V7.2.4 software. Results. Normal monocytes were differentiated to macrophages in vitro in the presence of sera from 24 untreated CLL patients with different prognostic factors (genomic aberrations, % CD38 and IGHVmutational status). About 45% of the CLL sera (N=10; 6 M-CLL, 4 U-CLL) drove macrophage maturation toward an M2-like phenotype, as assessed by surface expression of CD23, CD64, CD32, CD36, MRC1, etc. These 10 sera induced higher CD23 expression after 3 days in culture compared to AB human serum, whereas the levels of M1-specific markers (CD64 and CD32) did not change relative to the control. Interestingly all of these 10 CLL sera came from patients bearing 13q14 Δ (N=5), 17p13 Δ (N=3) or a combination of these (13q14 Δ + 17p13 Δ; N=1) and 17p13 Δ + trisomy12; N=1)). On the contrary, no increase in CD23 expression was detected in presence of sera from patients with 11q22 Δ (N=1) alone or in combination with 13q14 Δ (13q14 + 11q22 Δ; N=5). Of note, treatment with a neutralizing mAb specific for IL-4 did not block the CLL serum induced up-regulation of CD23 (N=2). In a parallel set of studies, normal monocytes were incubated with each of the 24 CLL sera in combination with the M1 promoting cytokine, IFNg or the M2 promoting cytokine, IL4. In all cases IL4 induced CD23 up-regulation and an M2 phenotype. Paradoxically, IFNg, which normally induces an M1 phenotype, also induced an M2 phenotype (i.e., enhanced CD23 expression) when co-cultured with sera from a subset patients (N=8; 6 M-CLL and 2 U-CLL). Of note, the IFNg stimulatory effect on CD23 expression was observed with a different set of sera from those that directly stimulated CD23 expression. Furthermore, CD64 expression did change after incubation with IFNg + CLL serum in 6 of 8 cases, yielding another unusual (CD23+CD64+) macrophage phenotype. The 2 sera that did not yield such hybrids were from M-CLL patients. Conclusions. Sera from CLL patients contain two apparently novel activities that mature normal monocytes to M2-like macrophages. The first acts directly by an action that is apparently independent of IL-4 and associates with 13q14 Δ or 17p13 Δ abnormalities. The second acts indirectly through IFNg and leads to macrophages with a hybrid M2/M1 phenotype (CD23+CD64+), suggestive of a new type of macrophage. Disclosures No relevant conflicts of interest to declare.
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Lu, Kristina T., Frank L. Sinquett, Rebecca L. Dryer, Charles Song, and Lori R. Covey. "c-Rel plays a key role in deficient activation of B cells from a non–X-linked hyper-IgM patient." Blood 108, no. 12 (December 1, 2006): 3769–76. http://dx.doi.org/10.1182/blood-2006-03-008839.
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AbstractOur previous results demonstrated that B cells from a patient (pt1) with non–X-linked hyper-IgM syndrome (HIGM) possess an atypical CD23lo phenotype that is unaffected by CD40-mediated activation. To investigate the molecular mechanism underlying defective CD23 expression in pt1 B cells, we used lymphoblastoid cell lines that express LMP1 under the control of a tetracycline-inducible promoter (LCLtet). Our analysis revealed that the CD23lo phenotype in the pt1-LCLtet cells is a direct consequence of diminished CD23 transcription. We demonstrate a marked decrease in c-Rel–containing complexes that bind to the proximal CD23a/b promoters in pt1-LCLtet extracts, resulting from an overall lower expression of c-Rel in pt1-LCLtet cells. Analysis of c-Rel mRNA revealed relatively equal amounts in pt1-LCLtet and control LCLtet cells, indicating that diminished c-Rel protein expression is unrelated to decreased transcription. Finally, a critical role for c-Rel in CD23 regulation was demonstrated by effectively altering c-Rel expression that resulted in the direct modulation of CD23 surface expression. Collectively, these findings demonstrate that low levels of c-Rel are the underlying cause of aberrant CD23 expression in pt1 B cells and are likely to play a critical role in the pathophysiology of this form of HIGM.
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Nambu, Mitsuhiko, Michael Hagen, Matyas Sandor, Randy E. Sacco, KyuBum Kwack, and Richard G. Lynch. "Functional significance of CD23- on CD23-transfected Th2 clone." Immunology Letters 44, no. 2-3 (January 1995): 163–67. http://dx.doi.org/10.1016/0165-2478(94)00209-a.
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