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Academic literature on the topic 'CD23'

Author: Grafiati

Published: 4 June 2021

Last updated: 14 February 2022

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Journal articles on the topic "CD23"

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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Dissertations / Theses on the topic "CD23"

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Shi, Jianguo. "Interaction of human CD23 with IgE and CD21." Thesis, King's College London (University of London), 1997. https://kclpure.kcl.ac.uk/portal/en/theses/interaction-of-human-cd23-with-ige-and-cd21(373685f2-b918-4cae-9404-c10d226ff134).html.

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Van, Zyl Dwain George. "Production of recombinant human CD21 and CD23 : towards a better understanding of their interaction." Thesis, Nelson Mandela Metropolitan University, 2013. http://hdl.handle.net/10948/d10211135.

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The prevalence of allergic diseases has dramatically increased over the last three decades. Presently, it is estimated that 20-30 per cent of the developed world suffers from allergic diseases. The majority of allergic diseases are rooted in the activities of IgE; an immunoglobulin which exerts its effector functions by interacting with a network of proteins. This network includes its low affinity receptor CD23. Cross linking of membrane IgE and CD21 by soluble CD23 results in an increase in IgE synthesis. This marks the interaction between CD23 and CD21 as an attractive therapeutic target. However, details regarding this interaction are inadequate for rational drug design. To obtain a deeper understanding of the CD23-CD21 interaction recombinant human CD21 (SCR1-2 and SCR5-8) and CD23 (16 kD and 25 kDa) were produced. The cloning, expression and purification of recombinant proteins comprised a significant portion of this study. Recombinant CD23 was expressed as inclusion bodies, refolded by rapid dilution and purified by size exclusion chromatography. Conversely, recombinant CD21 was expressed as soluble MBP-fusions and purified with an amylose affinity resin. The interaction between recombinant CD23 and CD21 was analysed by flow cytometry and ELISA experiments. Flow cytometry showed that 16 kDa and 25 kDa CD23 interacted with SCR5-8 to the same extent. Semi-quantitative ELISA experiments showed that both SCR1-2 and SCR5-8 were able to interact with 16 kDa and 25 kDa CD23. This suggests that the binding sites of SCR1-2 and SCR5-8 occur on 16 kDa CD23. Furthermore, since proteins were expressed in E. coli it suggests that the CD23-CD21 interaction does not require glycosylation. Furthermore, considering what is known about the SCR1-2-CD23 interaction from previous NMR studies; i.e. that the C-terminal tail (residues residues 289-298) of CD23 is responsible for binding SCR1-2, indicates that SCR5-8 binds somewhere within the lectin domain of CD23. This indicates that the CD23-CD21 interaction involves C-terminal tail-SCR1-2 and lectin domain-SCR5-8 interactions.

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Yahya, Mohd Norhakim. "Analysis of the IgE network : inhibition of CD23-mediated IgE upregulation and CD21/C3d interaction." Thesis, University of Oxford, 2011. http://ora.ox.ac.uk/objects/uuid:bc5ff165-2d2c-4e4f-a0e9-5651cacd2ddf.

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Allergic reactions are mainly mediated by the interactions between the IgE and its ligands, amongst them CD23 and CD21 in what is termed the IgE network. CD23 is involved in upregulating IgE expression by forming a trimolecular complex with CD21 and IgE on the B-cell surface, resulting in the specific activation of IgE-positive B cells. CD21 also interacts with C3d and is a bridge between the innate and the immune system. A crystal structure of the interaction has been solved (Szakonyi et al., 2001) but was controversial because it contradicted previous biochemical analyses. The aims of this thesis were to use various biophysical techniques to study the interactions between the molecules in the IgE network and its possible inhibition. Part 1: Characterisation of a phage display-derived peptide that inhibit IgE binding to CD23 A peptide was previously derived using phage display technology and tested for binding ability to CD23 using SPR and ITC. Subsequent NMR experiments were performed to identify the binding site, followed by characterization of its derivatives. Crystallisation of CD23 with the peptide and soaking with its truncated tripeptide, NWP, were also attempted. Part 2: Characterisation of CD23 and its interaction with its ligands X-ray crystallography was undertaken to solve the structure of derCD23 in complex with a phage display-derived peptide (Part1) followed by crystal soaking with a truncated tripeptide, NWP. However, a reproducible, high-resolution wild type derCD23 structure was determined at 1.9 Å. A comparison of the binding behaviour between the monomeric derCD23 and a trimeric CD23 construct was carried out in order to see the effect of oligomerisation upon IgE binding. Using the known interaction map as well as a crystal structure, the possible interacting residues between CD23 and IgE were examined. The characterisation of the CD23/CD21 interaction was continued from previous efforts in order to confirm that the binding epitope of CD23 for CD21 lies within the C-terminus of CD23. Characterisation of the interactions of CD23/IgE/FcεRI was performed to examine these multimolecular interactions and possible regulatory mechanisms in mast cell degranulation. It was shown that CD23 can form multimeric complexes with IgE-Fc that bind to FcεRI with higher apparent affinity than IgE-Fc alone, which may lead to increases in mast cell degranulation. It was also found that the IgE bound on FcεRI still binds to CD23 although with a lower binding capacity, presumably due allosteric changes. The binding of CD23 with a monoclonal antibody IDEC-152 was also characterised using SPR and NMR spectroscopy. It was proposed that IDEC-152 might interfere with the trimerisation site of CD23 thus reducing its affinity for IgE. A thermofluor assay was developed and optimised for potential screening of compounds that bind to derCD23 using a qPCR machine, which may be useful to screen compounds that bind to CD23 as part of future drug discovery project. Crystallisation of the derCD23/CD21 and IgE/triCD23/CD21 complexes was also attempted as part of ongoing crystallisation projects. Part 3: The interaction between C3d and CD21 The interaction between C3d and CD21 is believed to be a bridge between the innate and adaptive immune response, and is thought to be pivotal in the initiation of autoimmune disease. Following from previous studies on this interaction, further characterisations were performed using NMR and ITC to confirm the involved sites on CD21 (SCR1-2) in binding to C3d. Several potential salt bridges have been identified so far, allowing a high-resolution docked structure of the C3d/CD21 complex.

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Karagiannis, Sophia. "The process of endocytosis of CD23." Thesis, King's College London (University of London), 1995. https://kclpure.kcl.ac.uk/portal/en/theses/the-process-of-endocytosis-of-cd23(553202e7-a9c8-444e-b0a5-f7561d1e6297).html.

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Ford, Jill Wallace. "CD23's Role as a Negative Regulator of Allergic Disease: in vivo Effects of Murine CD23 Destabilization and Allelic Mutations." VCU Scholars Compass, 2007. http://hdl.handle.net/10156/2104.

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Grundy, Gabrielle Jane. "The structure and function of human soluble CD23." Thesis, King's College London (University of London), 2001. https://kclpure.kcl.ac.uk/portal/en/theses/the-structure-and-function-of-human-soluble-cd23(1c2f66b1-b335-4192-892f-bbbf3afde432).html.

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Yuan, Daopeng. "Structural studies of human CD23 and its complexes." Thesis, King's College London (University of London), 2012. https://kclpure.kcl.ac.uk/portal/en/theses/structural-studies-of-human-cd23-and-its-complexes(b8946602-66b9-4b39-a02e-4cda67c1c26d).html.

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IgE plays a central role in the pathogenesis of immediate hypersensitivity reactions through interacting with its receptors, in particular the high affinity receptor FcεRI. The low-affinity IgE receptor, CD23, affects IgE-dependent immune responses by regulating the synthesis of IgE, facilitating allergen presentation to the immune system, and influencing the activation and differentiation of B- and T-cells. Surprisingly, CD23 is different from other Ig receptors and belongs to the C-type (calcium-dependent) lectin family. Calcium binding to CD23 affects IgE binding to CD23, but previous NMR and crystal structures of CD23 gave conflicting results concerning the calcium binding sites. Investigation of calcium binding site(s) in CD23 and its complexes may assist CD23- targeted drug design. DerCD23 (a fragment of human CD23 that consists of the lectin domain and part of the C-terminal tail) and derCD23 mutants designed to remove each of the two potential calcium binding sites, were expressed and purified. The crystal structures of Ca2+-bound wild type derCD23, the complex with the Fcε3-4 sub-fragment of IgE-Fc, and four putative calcium binding site mutants of derCD23 were solved. Binding affinities of derCD23 and its mutants for calcium and for IgE-Fc were measured with ITC and SPR. The results indicate a loop of derCD23 (loop 4) is stabilized upon calcium binding to “site 2” and thereby contributes to the increased binding affinity for IgE. In addition, a residue (D258) in the non-conserved “site 1” is observed to bind IgE directly in the Ca2+-bound derCD23/Fcε3-4 complex. Thus, Ca2+ bound to site 2 in CD23 stabilizes loop 4 for IgE binding, whereas site 1 has evolved to bind IgE directly. Clinical studies of IDEC152 (also known as Lumiliximab), a primatized IgG1, anti- CD23 monoclonal antibody (IDEC Pharmaceuticals, San Diego, CA) show positive clinical effects in patients with allergic asthma and chronic lymphocytic leukemia. The Fab fragment of IDEC152 was prepared by enzymatic digestion from IDEC152 and crystals of the complex of derCD23 with IDEC152-Fab were grown, which diffracted to 2.4 Å resolution.

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Ilkow, Veronica Franciszka. "Engineering IgE antibodies and CD23 for therapeutic discovery." Thesis, King's College London (University of London), 2018. https://kclpure.kcl.ac.uk/portal/en/theses/engineering-ige-antibodies-and-cd23-for-therapeutic-discovery(54f73d64-5c16-42c4-9dea-42855873eeb6).html.

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Immunoglobulin E (IgE) is fundamental to the allergic response and the functions of IgE are mediated by its Fc region binding to two receptors, FcεRI and CD23 (FcεRII). The interaction of IgE with other proteins have complicated our investigations of the unique role each receptor plays. To solve this, a small-scale library of IgE-Fc proteins was designed with two key positions, one at each receptor-binding site mutated. The unpredictable allosteric nature of IgE prevents rational engineering approaches, thus the design of a membrane-bound IgE-Fc-GFP-tagged protein allowed for the generation of a membrane-surface display library of stable cell lines. A FACS selection assay identified IgE-Fc proteins with weakened binding to a single IgE-receptor, which serves as a proof-of-principle for this concept. Additional studies into human CD23 and the differences between it and murine CD23 revealed additional levels of regulation for IgE-binding not seen in other species and this is due to its unique properties. Human CD23 is an unusual antibody receptor, being a calcium dependent (C-type) lectin that has lost its carbohydrate binding capability. Ca2+ binds to and increases CD23’s affinity for IgE, and one of two Ca2+ binding sites usually present in C-type lectins is absent in human but present in murine CD23. To understand if the loss of the second Ca2+ binding site has led to a regulatory gain/loss of function in human CD23, a panel of CD23 mutant proteins with increasingly ‘mouse-like’ sequences was generated. The insertion of the second Ca2+ binding site was verified by HSQC-NMR whilst molecular dynamic simulations provided a means of understanding the flexibility of the proteins. It revealed that binding of two Ca2+ ions tethers the soluble CD23 loops into position in the most mouse-like mutant protein, limiting possible conformations for IgE binding. Complementary Biacore experiments indicated that higher calcium binding affinity may have come at a cost of weakened IgE binding, as data in the presence and absence of Ca2+ showed decreased binding affinities of the proteins for human IgE. This regulatory difference between murine and human soluble CD23 could inform the development of CD23/IgE inhibitor therapeutics for the treatment of allergy.

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Ferreira, Lauren. "Cytokine properties of CD23 on human Eosinophilic cells." Thesis, Nelson Mandela Metropolitan University, 2007. http://hdl.handle.net/10948/503.

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CD23, the low affinity IgE receptor, is expressed by various cell types and has numerous functions depending on the form of the protein, its interaction with various ligands and the type of cell involved. CD23 is pivotal in the regulation of IgE, with the soluble form involved in up-regulation, while the membrane bound form is involved in the down-regulation. It is clear why it is believed to be a central molecule in allergic responses, and a therapeutic target for the treatment of allergic disease. In this study a recombinant form of the entire extracellular domain of the protein, exCD23, was produced by PCR cloning and expressed in E. coli. His•Tag™s were introduced onto the C-terminus and N-terminus, respectively, in order to simplify the purification procedure. After renaturation and purification, the recombinant exCD23 bound IgE, indicating its activity. From the IgE binding studies it was established that the position of the tag did not influence the binding. GST•Tagged™ exCD23 was also produced in an attempt to increase the solubility of the recombinant protein, but this proved unsuccessful. Butyrate differentiated EoL-1 cells were treated with the Nterminal His•Tagged™ exCD23, and the protein appeared to suppress the secretion of the constitutively expressed cytokines, especially IL-8 and IFN- , when compared to untreated cells. In addition, treatment of the EoL-1 cells with exCD23 had a significant proliferative effect, but could not induce differentiation of this cell line into mature eosinophilic-like cells.

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Bansal, Amolak Singh. "The influence of HLA DR on soluble CD23 secretion and serum soluble CD23 as a marker of immune dysregulation in human disease." Thesis, University of Southampton, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.266381.

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Books on the topic "CD23"

1

Deavin, Andrew James. The heterogeneous nature of CD23. Birmingham: University of Birmingham, 1994.

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Roussou, Euthalia P. Soluble CD23 in connective tissue diseases. Birmingham: University of Birmingham, 1995.

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Ghaderi, Abbas Ali. Functional study of the low affinity IgE receptor (Fc[epsilon]RII/CD23) on human B lymphocytes. Birmingham: University of Birmingham, 1990.

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name, No. Ectopeptidases: CD13/aminopeptidase N and CD26/dipeptidylpeptidase IV in medicine and biology. New York, NY: Kluwer Academic/Plenum, 2003.

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Martin, Hildebrandt, ed. Dipeptidyl aminopeptidases in health and disease. New York: Kluwer Academic / Plenum Publishers, 2003.

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Compans, R. W., M. D. Cooper, T. Honjo, H. Koprowski, F. Melchers, M. B. A. Oldstone, S. Olsnes, et al., eds. CD4+CD25+ Regulatory T Cells: Origin, Function and Therapeutic Potential. Berlin, Heidelberg: Springer Berlin Heidelberg, 2005. http://dx.doi.org/10.1007/3-540-27702-1.

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Saoulli, Catherine. CD28-independent, TRAF2-dependent costimulation of resting T cells by 4-1BB ligand. Ottawa: National Library of Canada, 1998.

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Stunt, Richard John. The role of the cytoplasmic domain in the localisation of the CTLA-4 and CD28. Birmingham: University of Birmingham, 2002.

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Clarke, Ian David. The influence of fixation and proteolytic digestion on the immunohistochemical labelling of T-cells with CD43, CD3and UCHL1. [s.l: The Author], 1991.

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Kay, Lyndsey Sara. Anti-B-cell lymphoma activity mediated by CD3+CD4-CD8- T cells activated in vitro or in vivo. Ottawa: National Library of Canada, 2003.

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Book chapters on the topic "CD23"

1

Conrad, Daniel H. "CD23." In New Drugs for Asthma, Allergy and COPD, 206–9. Basel: KARGER, 2001. http://dx.doi.org/10.1159/000062190.

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Conrad, D. H. "Structure and function of CD23." In The Immunoglobulin Receptors and their Physiological and Pathological Roles in Immunity, 195–206. Dordrecht: Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-011-5018-7_18.

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Wang, F., H. Kikutani, S. Tsang, T. Kishimoto, and E. Kieff. "EBNA-2 Transactivation of CD23." In Epstein-Barr Virus and Human Disease • 1990, 43–46. Totowa, NJ: Humana Press, 1991. http://dx.doi.org/10.1007/978-1-4612-0405-3_5.

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Sarfati, M., S. Fournier, H. Ishihara, M. Armant, and G. Delespesse. "The CD23 Multifunctional Molecule and its Soluble Fragments (IgE-Binding Factors or Soluble CD23)." In Progress in Immunology Vol. VIII, 465–72. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-51479-1_61.

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Peter Rieber, E., Gerti Rank, Ingrid Köhler, and Susanne Krauss. "Membrane Expression of Fc∈RII/CD23 and Release of Soluble CD23 by Follicular Dendritic Cells." In Advances in Experimental Medicine and Biology, 393–98. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2930-9_66.

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Swendeman, S. L., and D. Thorley-Lawson. "Soluble CD23/BLAST-2 (S-CD23/Blast-2) and Its Role in B Cell Proliferation." In Current Topics in Microbiology and Immunology, 157–64. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-74006-0_21.

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Yasui, Teruhito, Hiroshi Fujiwara, Masato Kamanaka, Tsutomu Kawabe, Nobuaki Yoshida, Tadamitsu Kishimoto, and Hitoshi Kikutani. "The Roles Of CD40 And CD23 In IgE Regulation." In Advances in Experimental Medicine and Biology, 349–54. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4615-5855-2_49.

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Yodoi, J., M. Hosoda, Y. Maeda, S. Sato, M. Takami, and T. Kawabe. "FcεR2/CD23: Regulation and Functional Roles in Cell Activation." In Progress in Immunology, 724–31. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-83755-5_98.

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Waldschmidt, Thomas J., and Lorraine T. Tygrett. "The Low Affinity IgE Fc Receptor (CD23) Participates in B Cell Activation." In Advances in Experimental Medicine and Biology, 149–56. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3396-2_19.

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Rieber, E. P., U. Pirron, N. Endres, and J. C. Prinz. "Human Fc ε RII/CD23 in the Regulation of the Allergic Immune Response." In New Trends in Allergy III, 82–91. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-46717-2_10.

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Conference papers on the topic "CD23"

1

Rana, Seema, and Rajiv Tangri. "Anaplastic large cell lymphoma ALK negative vs. peripheral T cell lymphoma (NOS) - diagnostic dilemma." In 16th Annual International Conference RGCON. Thieme Medical and Scientific Publishers Private Ltd., 2016. http://dx.doi.org/10.1055/s-0039-1685354.

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Middle aged female presented with generalised lymphadenopathy and fever for last one month. Peripheral blood findings were within normal limits. There was no extra nodal involvement. FNAC performed initially from a cervical node suggested possibility of Hodgkin’s lymphoma and a whole node biopsy was performed. Histopathogical examination revealed effaced nodal architecture and a polymorphous population of lymphocytes, plasma cells, neutrophils and scattered large mononuclear cells with prominent nucleolus. An initial panel of CD3, CD20, LCA, CD15, CD30 and PAX5 was performed. The large atypical cells were positive for LCA, CD3 and CD30 with variable positivity for CD15. CD 30 showed Golgi and membranous staining. These large atypical cells were negative for PAX5 and CD20. In view of above findings, Hodgkin’s lymphoma was ruled out and a possibility of Non- Hodgkin’s lymphoma was considered. Further IHC markers were performed which included CD2, CD5, CD7, EMA, Alk, CD10 and KI67. CD5 showed variable positivity. The cells of interest were negative for CD2, CD7, ALK and EMA. Ki 67 index was 70-80%. Overall histological and IHC findings favoured Alk negative Anaplastic large cell lymphoma. Differential diagnosis considered was peripheral T cell lymphoma (NOS). Hodgkin’s lymphoma, peripheral T cell lymphoma (NOS) and anaplastic large cell lymphoma share common histomorphological findings. With careful analysis of Immunohistochemistry, it is easier to categorise Hodgkin’s lymphoma. ALK negative anaplastic large cell lymphoma and peripheral T cell lymphoma (NOS) are difficult to categorise and show overlapping features. We in this case have discussed clinical, histomorphological and IHC pattern of Alk negative Anaplastic large cell lymphoma.

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Chichkova, Nathalia, Vladimir Fisenko, and Evgenii Gitel. "Asthma and chronic rhinosinusitis: comparative evaluation of IgE plasma level, CD23+ and blood eosinophils." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa663.

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Mukherjee, Kalyan K., Debasish Banerjee, Anjan Das, Subham Halder, Dattatreya Mukherjee, Shyam S. Mondal, Surya K. Roy, Mili Das, Chinmay K. Panda, and Utpal Chaudhuri. "Significance of Detecting Minimal Residual Disease by Flow Cytometry and its Impact on Overall Survival and Prognosis of Pediatric B-Cell ALL Patient Experience from a Tertiary Care Centre in Eastern India." In Annual Conference of Indian Society of Medical and Paediatric Oncology (ISMPO). Thieme Medical and Scientific Publishers Pvt. Ltd., 2021. http://dx.doi.org/10.1055/s-0041-1735366.

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Abstract Introduction The improved prognosis of pediatric B-cell acute lymphoblastic leukemia (pBALL) is considered as a good progress of medical science in the field of oncology and hematology. Minimal residual disease (MRD) refers to presence of disease in molecular level is a newer practice with respect to the detection of complete remission by conventional pathologic analysis. Prognostic value of MRD in pediatric ALL (p-ALL) is well known. Objectives This study was aimed to describe clinical outcomes and prognosis, that is, overall survival and relapse in the patients with pBALL with respect to minimal residual disease detection on day 15, day 29, and postconsolidations in a tertiary care center in eastern India. Materials and Methods Eight color flow cytometry was used to detect MRD in this study. This contained markers such as CD 19, CD 34, CD 10, CD58, CD 45, CD13, anti-TDT, CD33. Eight panels included were (1) CMPO-FITC/cCD79a-PE/cCd3ECD, (2) CD20-FITC/cCD10-PE/cCd-19ECD, (3) CD34-FITC/cCD117-PE/cCd45 ECD/CD2 PC 5, (4) CD15 FITC/CD33PE/CD45ECD, (5) CD14 FITC/CD13 PE/CD45ECD, (6) HLADR FITC/CD7 PE/CD45 ECD, (7) TdT FITC/CD45 ECD (IF CD34 NEG), and (8) CD58 FITC/CD 45 ECD (IF BOTH CD34 AND TdT NEG; were used to prepare the marker. Results The study included 52 patients. In the 52 patients, 59.6% patients are alive with a p-value of 0.031. MRD was checked on every 15th and the 29th day and postconsolidation of the treatment where in day 15 (p = 0.023), it was 53.4% positive and 46.5% negative. On day 29 (p = 0.031), MRD was 22.5% positive and 77.5% negative, in post consolidation, it was positive in 20% and negative is 80%. MRD value below 0.01 is taken as negative and above is taken as positive. The overall survival (OS) is of 32.88 + 8.59 with a 6 to 36 months of duration. In In relapsed cases, no hemorrhagic relapse was found and two CNS relapse were found. Conclusion It was a study of 52 patients of pBALL with a detection of MRD by FCM. MRD-negative patients had a good prognosis and comparatively lower rate of relapse than the one with positive MRD. Effort should be made to adhere to recommendation of MRD testing in clinical guidelines.

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Harris, Sarah, James Woodworth, Julie Ranuio-Kelley, Annalee Estrellado, Alessandra Cesano, Hua Mu, and Shabnam Tangri. "Abstract LB-305: Soluble CD23 levels increase following lumiliximab dosing in relapsed chronic lymphocytic leukemia patients." In AACR Annual Meeting--Apr 12-16, 2008; San Diego, CA. American Association for Cancer Research, 2008. http://dx.doi.org/10.1158/1538-7445.am2008-lb-305.

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Efanov, Alexey A., Nicola Zanesi, Vadim Maximov, Natalya Nazaryan, Urmila Santanam, Alexey Palamarchuk, Carlo M. Croce, and Yuri Pekarsky. "Abstract 401: CD5+CD23+ leukemic cell populations in Tcl1 transgenic mice show significantly increased proliferation and Akt phosphorylation." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-401.

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Cai, Wenyan, Jianbo Dong, Sachith Gallolu Kankanamalage, Allison Titong, Jiadong Shi, Zhejun Jia, Bo Wang, et al. "Abstract LB068: A novel CD20/CD3 T cell engager designed from Rituximab targeting CD20+ cancer with multiple mechanisms." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-lb068.

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Lupia, Michela, Giovanni Bertalot, Pier Paolo Di Fiore, Nicoletta Colombo, Fabrizio Bianchi, and Ugo Cavallaro. "Abstract A66: The CD73+/CD24- subpopulation of ovarian cancer cells is enriched in cancer stem cells." In Abstracts: AACR Special Conference: Advances in Ovarian Cancer Research: Exploiting Vulnerabilities; October 17-20, 2015; Orlando, FL. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1557-3265.ovca15-a66.

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Feulner, Julian, Michael Aigner, Roman Kischel, Peter Kufer, Patrick A. Baeuerle, Andreas Mackensen, and Stefan W. Krause. "Abstract 4622:A novel CD33/CD3-bispecific BiTE antibody can effectively recruit autologous T cells from AML-patients for in vitro cell lysis of CD33+blasts." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-4622.

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Krupka, Christina, Peter Kufer, Roman Kischel, Gerhard Zugmaier, Thomas Köhnke, Felix Lichtenegger, Torben Altmann, et al. "Abstract B070: Characterization of covariables modulating CD33/CD3 BITE® antibody construct mediated cytotoxicity against primary AML cells." In Abstracts: CRI-CIMT-EATI-AACR Inaugural International Cancer Immunotherapy Conference: Translating Science into Survival; September 16-19, 2015; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr15-b070.

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Comeau, Michael R., Danielle Mitchell, Rebecca Gottschalk, Lynda Misher, Mollie Daugherty, Lara Parr, Peter Pavlik, et al. "Abstract 597: Bispecific anti-CD123 x anti-CD3 ADAPTIR™ molecules for redirected T-cell cytotoxicity in hematological malignancies." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-597.

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Reports on the topic "CD23"

1

Mekova, Ralitsa V., Spaska S. Lesichkova, Adelina D. Tsakova, Julieta Z. Bakalova, Deniz Bakalov, and Mihail Boyanov. Circulating CD3(+)CD4(+)CD28(‒) T Lymphocytes in Patients with Autoimmune Thyroiditis. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, May 2020. http://dx.doi.org/10.7546/crabs.2020.05.14.

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Fitzgerald, David. Anti-CDR3 Therapy for B-Cell Malignancies. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada619137.

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Fitzgerald, David. Anti-CDR3 Therapy for B-Cell Malignancies. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada590597.

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Zheng, Pan. CD24 as a Potential Therapeutic Target in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, April 2009. http://dx.doi.org/10.21236/ada508268.

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Shelley, Carl S. Determination of the Molecular Mechanisms Responsible for Abnormal CD43 Expression in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2001. http://dx.doi.org/10.21236/ada396321.

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