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Journal articles on the topic 'Lymphocytes'
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Klein, Ami, Michael Lishner, Barbara Bruser, John E. Curtis, Dominick J. Amato, and Aaron Malkin. "Cortisol catabolism by lymphocytes of patients with chronic lymphocytic leukemia." Biochemistry and Cell Biology 68, no. 4 (April 1, 1990): 810–13. http://dx.doi.org/10.1139/o90-118.
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A low rate of catabolism of cortisol by lymphocytes correlates with high sensitivity of the cells to the steroid and causes them to die at a greater rate than control samples. Since lymphocytes of patients with chronic lymphocytic leukemia respond to treatment with glucocorticosteroids and are cortisol sensitive, we attempted to see whether their capability to catabolize cortisol differs from that of normal lymphocytes. No difference was found between the two groups of cells with regard to the pattern of cortisol metabolites. However, the lymphocytes of the chronic lymphocytic leukemia groups showed a total cortisol catabolism per cell that was significantly lower than that of the control group. Patients with low lymphocyte count in peripheral blood showed a relatively higher cortisol metabolism by lymphocytes per cell than those with high counts.Key words: lymphocytes, cortisol, catabolism, chronic lymphocytic leukemia, morbidity.
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Spain, B. A., D. M. Soliman, R. A. Sidner, and H. L. Twigg. "Enhanced proliferation and IL-2 secretion by lung lymphocytes from HIV-infected subjects." American Journal of Physiology-Lung Cellular and Molecular Physiology 269, no. 4 (October 1, 1995): L498—L506. http://dx.doi.org/10.1152/ajplung.1995.269.4.l498.
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Human immunodeficiency virus (HIV)-positive patients frequently develop a CD3+/CD8+ cytotoxic T cell lymphocytic alveolitis. This could occur through in situ expansion of lung lymphocytes. We evaluated lung and blood lymphocyte proliferation in asymptomatic HIV-infected individuals by measuring spontaneous and cytokine-induced tritiated thymidine incorporation. Interleukin (IL)-2 and IL-4 secretion was determined with the use of enzyme-linked immunosorbent assay, Western blotting, and immunoprecipitation techniques. Spontaneous proliferation by lung lymphocytes from HIV-positive patients was significantly greater than that of normal volunteers. Proliferation was confined to the CD8+ lymphocyte subset. Over time, spontaneous proliferation declined unless autologous alveolar macrophages (AM) were added, suggesting AM were providing additional stimulatory signals to lung lymphocytes. Lung and blood lymphocytes proliferated in response to IL-2 but not IL-4. Lymphocytes in HIV-infected lung spontaneously produced and secreted more IL-2 than either normal lung lymphocytes or autologous blood lymphocytes. IL-4 production was not detectable in either group. These findings support the hypothesis that lymphocytic alveolitis in asymptomatic HIV-positive patients results from IL-2-dependent in situ proliferation of CD3+/CD8+ cytotoxic T cells.
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Chen, Lin-Ying, Julia Y. S. Tsang, Yun-Bi Ni, Siu-Ki Chan, Kui-Fat Chan, Sheng Zhang, and Gary M. Tse. "Lymphocyte subsets contribute to the degree of lobulitis and ductitis in sclerosing lymphocytic lobulitis of the breast." Journal of Clinical Pathology 69, no. 6 (November 18, 2015): 527–32. http://dx.doi.org/10.1136/jclinpath-2015-203334.
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AimsSclerosing lymphocytic lobulitis (SLL) of the breast is characterised by lymphocytic lobulitis, ductitis, vasculitis and dense keloidal fibrosis with epithelioid fibroblasts. However, the subsets of the infiltrating lymphocytes and their contribution to disease progression have not been fully explored.MethodsCD20, CD3, CD4, CD8 and regulatory T (Treg) lymphocytes were evaluated in the epithelial and vascular areas in SLL. The relationship between the lymphocyte subset in different regions and the degree of inflammation was analysed.ResultsLymphocytic infiltration was mainly located in peri-lobular, peri-ductal and peri-vascular areas. No significant differences between CD20 and CD3 lymphocytes were found in peri-epithelial areas. However, there were more intra-ductal/lobular epithelial CD3 than CD20 lymphocytes (p<0.001). For T lymphocyte subsets, more CD4 than CD8 lymphocytes were found in the peri-lobular/vascular regions (p≤0.026); but an opposite trend was seen in the intra-ductal/lobular regions (p<0.001). In the peri-lobular/vascular regions, generally, different lymphocyte subsets correlated with each other. Interestingly, in the peri-ductal region, only CD4 lymphocytes showed significant correlations with all other subsets (p≤0.020). Regarding their relationship with the degree of inflammation, significant positive correlations were observed for all subsets in peri-vascular/lobular regions (p≤0.045). Only regulatory T cells, but not the others, at the peri-ductal region showed significant correlation with the degree of inflammation at all three regions (p≤0.014).ConclusionsIn addition to B lymphocyte subsets, T lymphocyte subsets could be involved differently in SLL. CD4 lymphocytes may have a pivotal role in recruiting other subsets to the inflamed site, and triggered the cascade of inflammatory changes resulting in fibrosis.
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Raje, Manoj, and Karvita B. Ahluwalia. "Motility of leukemic lymphocytes." Proceedings, annual meeting, Electron Microscopy Society of America 48, no. 3 (August 12, 1990): 368–69. http://dx.doi.org/10.1017/s0424820100159382.
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In Acute Lymphocytic Leukemia motility of lymphocytes is associated with dissemination of malignancy and establishment of metastatic foci. Normal and leukemic lymphocytes in circulation reach solid tissues where due to in adequate perfusion some cells get trapped among tissue spaces. Although normal lymphocytes reenter into circulation leukemic lymphocytes are thought to remain entrapped owing to reduced mobility and form secondary metastasis. Cell surface, transmembrane interactions, cytoskeleton and level of cell differentiation are implicated in lymphocyte mobility. An attempt has been made to correlate ultrastructural information with quantitative data obtained by Laser Doppler Velocimetry (LDV). TEM of normal & leukemic lymphocytes revealed heterogeneity in cell populations ranging from well differentiated (Fig. 1) to poorly differentiated cells (Fig. 2). Unlike other cells, surface extensions in differentiated lymphocytes appear to originate by extrusion of large vesicles in to extra cellular space (Fig. 3). This results in persistent unevenness on lymphocyte surface which occurs due to a phenomenon different from that producing surface extensions in other cells.
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Hrushik, Amin, Lisa Thomas, Qi Shi, Sudeep Ruparelia, Alfonso Zangardi, and Howard Nash. "Chronic Lymphocytic Leukemia with Bi-Nucleated Lymphocytes." Blood 126, no. 23 (December 3, 2015): 5285. http://dx.doi.org/10.1182/blood.v126.23.5285.5285.
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Abstract Introduction: B-cell chronic lymphocytic leukemia is one of the common lymphoproliferative disorders in the adult patient population. It is very uncommon to find bi-nucleated lymphocytes as a morphological feature in this disorder. Our patient was diagnosed with CLL and was found to have bi-nucleated lymphocytes in the peripheral smear. The mechanism behind this type of morphological feature of lymphocytes is unknown in CLL, and whether it has prognostic value on disease outcome is undetermined. Case Description: 62 y/o man was referred to hematology oncology after diagnosis of small cell lymphocytic leukemia was made s/p a right inguinal lymph node biopsy. His CBC revealed a wbc count of 14,000, Rbc count of 4,360, Absolute lymphocyte count of 11,500 and Platelet count of 125,000. The patient did not have any B-symptoms. On physical exam, a pertinent finding was palpable right axillary adenopathy. The CT of abdomen /pelvic to evaluate these findings. This revealed extensive axillary, abdominal/pelvic lymphadenopathy, hepatosplenomegaly and cardio phrenic lymphadenopathy. The patient had a biopsy of the right inguinal lymph node as well as bone marrow biopsy. Biopsy results showed small lymphocytic cells, some of which show occasional large nucleoli were consistent with small lymphocytic lymphoma/chronic lymphocytic leukemia, and morphologic characteristics of the lymphocytes showed bi-nucleated lymphocytes in peripheral blood smear (figure A). Flow cytometric analysis confirmed a lymphocytic population with lambda light chain restriction, expressing CD5, CD19, CD20, and CD23 consistent with chronic lymphocytic leukemia/small lymphocytic lymphoma. Bone marrow biopsy showed a hypercellular marrow with 75 % cellularity mainly composed of mature lymphocytes with scattered macrophages and eosinophils, Flow cytometric analysis (Clarient FI11-041053) of the bone marrow is interpreted as chronic lymphocytic leukemia/small cell lymphoma with the abnormal B cells representing 56% of the viable white cells. FISH study showed deletion of the ATM gene (11q22-23), D13S319 (13q14) and TP53 (p53) were observed in 29%, 71% and 35.5% of the cells analyzed, respectively. A subset of cells with the 13q deletion (20.5% of the total cells) showed homozygous deletion of D13S319 (13q14). ATM deletion is associated with progressive disease and poor prognosis in cases of chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL).He did not have any other previous history of malignancy or hematologic disorder. Discussion: B-cell chronic lymphocytic leukemia is one of the common lymphoproliferative disorders in the adult patient population. To make a diagnosis requires absolute lymphocyte count >4x10 9 and lymphoid cell morphology. In CLL, leukemic cells are small and mature appearing lymphocytes, which have regular nuclear and cytoplasmic outlines and scant weakly basophilic cytoplasm. Surface markers that define a CLL cell are proteins such as antibody light chains (kappa or lambda) and CD proteins (CD5, CD19, CD20, and CD23). In our patient absolute lymphocyte count was 11.5x109 and lymphocytic population showed surface marker lambda light chain and CD proteins CD5, CD19, CD20 and CD23 which was consistent with CLL/SLL on inguinal lymph node biopsy, but morphology of lymphocytes was small and mature bi-nucleated lymphocytes, which is very uncommon. Although bi-nucleated lymphocytes are described in a disorder "Polyclonal chronic B-cell lymphocytosis with bi-nucleated lymphocytes". Detection of an extra chromosome for the long arm of chromosome 3 +i(3)(q10) has been considered a specific marker of Polyclonal B-cell lymphocytosis with binucleated lymphocytes (PPBL),which was not present in our case. One case study by Amouroux et al, included four patients with B-cell CLL who were found to have bi-nucleated lymphocytes. Disease course was stable in one patient, one patient had an indolent course and only one required treatment due to rapid doubling time of lymphocytes. Our patient initiated chemotherapy with Rituxan and Fludara, as he had progressive disease with hepatosplenomegaly, lymph nodes and bone marrow involvement. Conclusion: Bi -nucleated lymphocytes in B-cell CLL are very rare. Explanations as to the etiology of this morphological feature in B-cell CLL is unknown. There is no sufficient evidence that bi-nucleated lymphocytes in CLL has any impact on disease progression. Disclosures No relevant conflicts of interest to declare.
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Choccalingam, Chidambharam. "Volume, conductance, and scatter parameters of neoplastic and nonneoplastic lymphocytes using Coulter LH780." Journal of Laboratory Physicians 10, no. 01 (January 2018): 085–88. http://dx.doi.org/10.4103/jlp.jlp_65_17.
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Abstract PURPOSE: Automated hematology analyzers yield a complete hematological profile including a complete blood count and a differential white blood cell count. The differential count is based on analyses of three parameters, namely, volume, conductance, and scatter (VCS). We aimed to evaluate the VCS parameters, histograms, and scatterplots of neoplastic and nonneoplastic lymphocytes. MATERIAL AND METHODS: Patients were grouped into four categories, namely, acute lymphoblastic leukemia (ALL), chronic systemic disorders, chronic lymphocytic leukemia (CLL), and acute viral disease. Lymphocytes from all four groups were compared with lymphocytes from normal participants. RESULTS AND CONCLUSIONS: The histogram for acute viral disease showed a trough at T1, which was slightly obliterated, and the F1 curve mildly extended to the right. The T1 for ALL was replaced with a peak at >40% of the preset limit. The F1 peak was shifted to left for CLL. The scatterplot for viral disease showed lymphocytes extending to the variant lymphocyte window. The lymphocytes of ALL extended to the blast window, with both increase in volume and mild increase in scatter. The lymphocytes in CLL were smaller and located below the normal lymphocyte region. Mean lymphocyte volume was significantly increased in ALL and was significantly decreased in CLL. Mean lymphocyte conductance was significantly increased in CLL and significantly decreased in both acute viral disease and ALL. Mean lymphocyte scatter was significantly decreased in acute viral disease and significantly increased in ALL.
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Wiley, J. S., J. R. Chen, G. P. Jamieson, and P. J. Thurlow. "Agonists for endothelial P2 purinoceptors trigger a signalling pathway producing Ca2+ responses in lymphocytes adherent to endothelial cells." Biochemical Journal 311, no. 2 (October 15, 1995): 589–94. http://dx.doi.org/10.1042/bj3110589.
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Recirculation of lymphocytes through the body involves their frequent adhesion to endothelial cells but little is known of the signalling pathways between these two cell types. Lymphocytes from patients with chronic lymphocytic leukaemia were loaded with the Ca(2+)-sensitive indicator, fura 2, and allowed to adhere to either glass or monolayers of human umbilical-vein endothelial cells. Addition of ATP or UTP (1-10 microM) to the superfusate produced a transient rise in cytosolic Ca2+ concentration in the lymphocytes adherent to endothelium (24 of 35 cells). In contrast, ATP or UTP (1-10 microM) had no effect on the cytosolic Ca2+ of lymphocytes attached to glass. As the only lymphocyte receptor for ATP (P2Z class) requires higher ATP concentrations (> 50 microM) for Ca2+ influx and is unresponsive to UTP, the involvement of a lymphocyte P2Z purinoceptor is unlikely. Various agonists including ATP, UTP, 2-methylthioATP, ADP and histamine all stimulated increases in endothelial cytosolic Ca2+ but only ATP and UTP (both agonists for endothelial P2U purinoceptors) triggered Ca2+ transients in adherent lymphocytes. Removal of extracellular Ca2+ did not abolish the ATP-induced rise in cytosolic Ca2+ concentration in lymphocytes adherent to endothelial cells. These findings show that stimulation of endothelial P2U purinoceptors triggers an endothelial-lymphocyte signalling pathway which releases internal Ca2+ in adherent lymphocytes.
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Winther, Birgit, Donald J. Innes, John Bratsch, and Frederick G. Hayden. "Lymphocyte Subsets in the Nasal Mucosa and Peripheral Blood during Experimental Rhinovirus Infection." American Journal of Rhinology 6, no. 4 (July 1992): 149–56. http://dx.doi.org/10.2500/105065892781874621.
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The local cellular response during rhinovirus infection was studied with immunohistochemical staining of lymphocyte subpopulations in the lamina propria of the nasal mucosa (inferior turbinate) in 25 biopsies from volunteers with experimental rhinovirus colds and compared with biopsies from healthy volunteers. Biopsies from rhinovirus infected volunteers, taken either in the early phase of the infection (days 3 and 5) or during convalescence (day 14) were evaluated in a semiquantitative fashion for degree of infiltration. Lymphocyte subpopulations also were counted on coded specimens. During experimental rhinovirus infection, no change could be observed in the overall degree of lymphocytic infiltration or in the numbers of T and B lymphocytes compared with control specimens. The overall degree of lymphocyte infiltration in the nasal mucosa was mild to moderate and consisted principally of T lymphocytes and only a few scattered B lymphocytes. Few natural killer lymphocytes were seen. These findings are similar to those in normal nasal mucosa and in contrast to the findings after topical application of recombinant interferon, which often results in a heavy lymphocyte infiltration. Lymphocyte subpopulation in the peripheral blood did not change when compared with prechallenge values in nine rhinovirus-infected volunteers.
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Li, Lijin, Sharon M. Dial, Monika Schmelz, Margaret A. Rennels, and Neil M. Ampel. "Cellular Immune Suppressor Activity Resides in Lymphocyte Cell Clusters Adjacent to Granulomata in Human Coccidioidomycosis." Infection and Immunity 73, no. 7 (July 2005): 3923–28. http://dx.doi.org/10.1128/iai.73.7.3923-3928.2005.
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ABSTRACT The in situ immunologic response in human coccidioidomycosis remains undefined. To explore this further, pulmonary necrotizing coccidioidal granulomata were examined using immunohistochemical staining for lymphocyte subsets and for the cytokines interleukin-10 (IL-10) and gamma interferon (IFN-γ). Discrete perigranulomatous lymphocytic clusters were seen in eight of nine tissues examined. In these tissues, T lymphocytes (CD3+) significantly outnumbered B lymphocytes (CD20+) in the mantle area of the granulomata (P = 0.028), whereas the clusters were composed of roughly equal numbers of T and B lymphocytes. While the number of cells in the mantle expressing IL-10 was similar to those in the perigranulomatous clusters, there were significantly more cells expressing IFN-γ in the mantle than in the clusters (P = 0.037). Confocal microscopy revealed that CD4+ T lymphocytes and B lymphocytes are associated with IL-10 production. CD4+CD25+ T lymphocytes were identified in the perigranulomatous clusters but were not associated with IL-10 production. This is the first report noting perigranulomatous lymphocyte clusters and IL-10 in association with human coccidioidal granulomata and suggests that down-regulation of the cellular immune response is occurring within coccidioidal granulomata.
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Zhang, Qiao-quan, Yan-fang Zhang, Nian Yu, Xing-jian Lin, and Qing Di. "Differential Diagnosis of Autoimmune Encephalitis from Infectious Lymphocytic Encephalitis by Analysing the Lymphocyte Subsets of Cerebrospinal Fluid." Analytical Cellular Pathology 2019 (December 3, 2019): 1–6. http://dx.doi.org/10.1155/2019/9684175.
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This study is aimed at investigating the lymphocyte subsets of cerebrospinal fluid (CSF) to provide possible differential diagnostic values and better understand the pathophysiological mechanism underlying autoimmune encephalitis (AE) and infectious lymphocytic encephalitis. A series of CD markers, including CD3/4/8/20 representing different types and developmental stages of lymphocytes, were used to count the corresponding subpopulations of CSF from clinical and laboratory confirmed cases of anti-N-methyl-D-aspartate receptor AE (NMDAR-AE), herpes simplex virus encephalitis (HSVE), and tuberculous meningitis (TBM). The percentages of lymphocytes observed and the CD4 : CD8 ratios were compared between the three groups. There were no significant differences of the percentage of total lymphocytes, CD3 cells, and CD4 cells of CSF among each group. However, there were strongly statistical differences of the CD4 : CD8 ratio in CSF of each group with 0.6 : 1 in NMDAR-AE, 0.9 : 1 in HSVE, and 3.2 : 1 in TBM. The percentage of CD20 B lymphocytes in NMDAR-AE was statistically higher than that of other groups. The distinct percentages of lymphocyte subpopulations of CSF appeared to be characteristic and could potentially serve as diagnostic indicators. Further verification and research will be necessary to clarify the significance and nature of CD4 : CD8 ratios and B lymphocytes in CSF between AE and the infectious lymphocytic encephalitis.
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Mirkamali, Mona, Hamid Reza Momeni, Tahereh Etemadi, Ghasem Mosayebi, and Majid Komijani. "Involvement of caspase-3 in apoptosis of human lymphocytes exposed to cadmium chloride." Human & Experimental Toxicology 41 (January 2022): 096032712211217. http://dx.doi.org/10.1177/09603271221121796.
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Background Lymphocytes are a group of white blood cells with a variety of roles their integrity is crucial for the body’s immune responses. Cadmium, a heavy metal and environmental pollutant, is known as a toxicant to exert its adverse effects on some sort of cells including blood cells. Research Design In this study, human lymphocytes were divided into 3 groups: (1) lymphocytes at 0-h, (2) lymphocytes at 24 h (control), (3) lymphocytes treated with cadmium chloride (15 μM). Lymphocyte viability and plasma membrane integrity were assessed in these groups. In addition, the occurrence of apoptosis was investigated by assessment of nucleus diameter and flow cytometry. Activation of caspase-3 was also detected by immunocytochemistry. Results Result showed that lymphocyte’s viability and plasma membrane integrity decreased in lymphocytes treated with cadmium as compared with the control group. Decreased nucleus diameter and result of flow cytometry demonstrated cadmium-induced apoptosis in human lymphocytes. Furthermore, lymphocytes treated with cadmium displayed intensely activated caspase-3 immunoreactivity in their cytoplasm. Conclusion In conclusion, cadmium not only negatively effect on viability and plasma membrane, but also induces caspase-dependent apoptosis in human lymphocytes.
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Schimpff, R. M., and A. M. Repellin. "In vitro effect of human growth hormone on lymphocyte transformation and lymphocyte growth factors secretion." Acta Endocrinologica 120, no. 6 (June 1989): 745–52. http://dx.doi.org/10.1530/acta.0.1200745.
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Abstract. Cultures of human blood peripheral lymphocytes were performed in the presence or absence of human growth hormone, and also of phytohemagglutinin and normal human serum 10%. After incubation for 48 h, the supernatants were tested for their ability to promote the uptake of [3H]thymidine into lectin-activated lymphocytes. Supernatants from lymphocyte-free control samples, treated in the same manner, were assayed under the same experimental conditions. Variance analysis of the different dose-response relationships was performed. The results of these in vitro experiments confirm that physiological levels of GH inhibit the lectin-induced lymphoproliferation and that lymphocytes secrete an 'activity' able to stimulate the incorporation of [3H]thymidine into lectin activated lymphocytes. Furthermore we show that: 1) Secretion of this lymphocyte-stimulating activity is increased by physiological levels of GH; 2) This lymphocytic secretion is not radioimmunoassayable IGF-I; 3) Using fast protein liquid chromatography (FPLC), this activity appears in fractions with various molecular weights.
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Twigg, Homer L., Blake A. Spain, Diaa M. Soliman, Kenneth Knox, Richard A. Sidner, Carol Schnizlein-Bick, David S. Wilkes, and Gary K. Iwamoto. "Production of interferon-γ by lung lymphocytes in HIV-infected individuals." American Journal of Physiology-Lung Cellular and Molecular Physiology 276, no. 2 (February 1, 1999): L256—L262. http://dx.doi.org/10.1152/ajplung.1999.276.2.l256.
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A CD8+lymphocytic alveolitis occurs in up to 60% of asymptomatic human immunodeficiency virus (HIV)-infected individuals. Early in HIV infection, lymphocytes consist predominantly of cytotoxic T lymphocytes directed against HIV-infected targets. As HIV disease progresses, they are replaced by CD8+CD57+suppressor cells. Virus-specific cytotoxic T lymphocytes secrete interferon-γ (IFN-γ), an important cytokine in upregulating immune responses, primarily through macrophage activation. We examined the ability of lung and blood lymphocytes from HIV-positive patients at various stages of HIV infection to secrete IFN-γ spontaneously and in response to phytohemagglutinin A. IFN-γ production and secretion were determined with ELISA, Western blot, immunoprecipitation, and Northern blot techniques. Lung lymphocytes from HIV-infected individuals secreted large amounts of IFN-γ. However, this ability was lost in patients with late-stage disease. Correlation between blood and lung lymphocyte IFN-γ secretion was poor, suggesting regional differences in lymphocyte function. These data suggest that lung levels of IFN-γ are high until late in HIV disease. These findings support the concept of administering exogenous IFN-γ to patients with late-stage HIV disease and opportunistic infections.
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Paschke, R., N. Brückner, R. Schmeidl, P. Pfiester, and K. H. Usadel. "Predominant intraepithelial localization of primed T cells and immunoglobulin-producing lymphocytes in Graves' disease." Acta Endocrinologica 124, no. 6 (June 1991): 630–36. http://dx.doi.org/10.1530/acta.0.1240630.
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Abstract. It has been proposed that intrathyroidal lymphocytes, localized in specific anatomical sites might have distinct, pathophysiologically relevant functions in Graves' disease. However, most studies of intrathyroidal lymphocytes were restricted to two lymphocyte locations and used semiquantitative methods. Therefore we used seven anatomically different lymphoid compartments to classify and evaluate by quantitative representative methods the total intrathyroidal lymphocytic infiltration and the staining indexes for immunoglobulin-producing plasmocytes and primed T cells (CD45RO), which provide maximum help to pokeweed mitogen-stimulated immunoglobulin synthesis in 36 thyroid glands from patients with Graves' disease. We found only 3.4% of all intrathyroidal lymphocytes intraepithelially. However, only intraepithelial lymphocytes showed a significantly higher staining index for primed T cells compared with several other compartments. There was also a high staining index for immunoglobulin-producing lymphocytes in this compartment. Kappa- and lambda-positive plasmocytes were found in a polyclonal distribution (kappa:lambda=64.1: 35.9) in all compartments. This increased incidence of CD45RO-positive T lymphocytes and of immunoglobulin-producing lymphocytes among the intraepithelial lymphocytes suggests a distinct pathophysiological function of lymphocytes in peripolesis in Graves' disease. Furthermore, there is a polyclonal intrathyroidal immunoglobulin synthesis.
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Silber, R., CM Farber, E. Papadopoulos, D. Nevrla, L. Liebes, M. Bruck, R. Brown, and ZN Canellakis. "Glutathione depletion in chronic lymphocytic leukemia B lymphocytes." Blood 80, no. 8 (October 15, 1992): 2038–43. http://dx.doi.org/10.1182/blood.v80.8.2038.2038.
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Abstract Glutathione (GSH) content may be the major determinant of a cell's sensitivity to cytotoxic alkylating agents. In the present study, the GSH concentration was determined in lymphocytes isolated from the blood of normal subjects and patients with chronic lymphocytic leukemia (CLL). Comparable levels were found in both types of cells. Incubation for 20 hours led to a decrease in GSH to 51% of baseline values in CLL B cells. Under the same conditions, normal B- or T-lymphocyte GSH content remained constant. GSH depletion was shown to be a characteristic of the B-CLL B lymphocyte. It was not found in the T cells of patients with B-CLL or in cells from patients with T-CLL. Chlorambucil (CLB) contributes to the decrease in GSH in B-CLL lymphocytes; after incubation with the drug, lower levels of GSH were found than in the normal B or T lymphocytes, B-CLL T cells, or T-CLL (CD4 or CD8) cells. GSH depletion of CLL B lymphocytes may be related to the greater therapeutic efficacy of CLB in B-CLL than in T-CLL.
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Silber, R., CM Farber, E. Papadopoulos, D. Nevrla, L. Liebes, M. Bruck, R. Brown, and ZN Canellakis. "Glutathione depletion in chronic lymphocytic leukemia B lymphocytes." Blood 80, no. 8 (October 15, 1992): 2038–43. http://dx.doi.org/10.1182/blood.v80.8.2038.bloodjournal8082038.
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Glutathione (GSH) content may be the major determinant of a cell's sensitivity to cytotoxic alkylating agents. In the present study, the GSH concentration was determined in lymphocytes isolated from the blood of normal subjects and patients with chronic lymphocytic leukemia (CLL). Comparable levels were found in both types of cells. Incubation for 20 hours led to a decrease in GSH to 51% of baseline values in CLL B cells. Under the same conditions, normal B- or T-lymphocyte GSH content remained constant. GSH depletion was shown to be a characteristic of the B-CLL B lymphocyte. It was not found in the T cells of patients with B-CLL or in cells from patients with T-CLL. Chlorambucil (CLB) contributes to the decrease in GSH in B-CLL lymphocytes; after incubation with the drug, lower levels of GSH were found than in the normal B or T lymphocytes, B-CLL T cells, or T-CLL (CD4 or CD8) cells. GSH depletion of CLL B lymphocytes may be related to the greater therapeutic efficacy of CLB in B-CLL than in T-CLL.
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Maslak, G. S., G. P. Chernenko, S. V. Abramov, I. Yu Pismenetska, I. V. Davydenko, L. M. Lushnya, and Makarets M. F. "Glycobiom Lymphocytes Surface Study of Patients with B-Cell Chronic Lymphocytic Leukemia." Ukraïnsʹkij žurnal medicini, bìologìï ta sportu 6, no. 6 (December 25, 2021): 134–40. http://dx.doi.org/10.26693/jmbs06.06.134.
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The purpose of the study was to investigate the intensity of exposure of peripheral blood lymphocyte surface glycans in patients with B-cell chronic lymphocytic leukemia by measuring the density of lectin- or antigen-positive epitopes under antitumor therapy in order to evaluate it for a more reasonable selection of qualitative and quantitative composition of therapy. Materials and methods. The objects of the study were blood lymphocytes of patients with chronic lymphocytic leukemia (n=15) aged 58-66 years before and after a course of standard chemotherapy according to the COP scheme. The control group consisted of healthy volunteers (n=15) aged 55 to 65 years. Isolation of lymphocytes was performed by a modified method of A. Boyum. Polyclonal antibodies to α1-acid glycoprotein and fibronectin were used. Exposure to Tn antigen and CD43 on blood lymphocytes was determined with secondary antibodies to mouse immunoglobulins conjugated to FITC (Millipore, USA). To study the exposure of glycans on the surface of lymphocytes, we used a set of seven lectins labeled with FITC. Data recording was performed on a Beckman Flower EPICS flow cytometer. Processing of the results was done using the program FCS3 Express. Results and discussion. Compared with the group of hematologically healthy donors on the surface of lymphocytes in patients with chronic lymphocytic leukemia, a 20-fold increase in the density of exposure to ConA epitopes, 10 times – UEAI- and SNA-positive epitopes were shown; MAA II epitope, Tn, and CD43 antigen densities were increased 100-fold (p <0.01). Exposure densities of MAA II-, Tn-, and CD43-positive epitopes on the plasma membrane of lymphocytes in patients with chronic lymphocytic leukemia receiving alkylation therapy decreased 10-fold relative to treatment data, but remained 10-fold higher than in the group of healthy hematologists. Conclusion. On the plasma membranes of lymphocytes in patients with chronic lymphocytic leukemia, the density of exposure of mannose and neuraminic acid residues was significantly increased. COP therapy reduced the density of these epitopes to control values. A significant increase in the density of carcinogenesis markers – Tn- and CD43-antigens on the plasma membranes of lymphocytes in patients with chronic lymphocytic leukemia has been shown. COP therapy provided only a partial decrease in their density, which indicates the insufficient effectiveness of COP therapy, its inability to completely stop the oncological process in patients with chronic lymphocytic leukemia
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Gagne, J. M., D. J. Weiss, and P. J. Armstrong. "Histopathologic Evaluation of Feline Inflammatory Liver Disease." Veterinary Pathology 33, no. 5 (September 1996): 521–26. http://dx.doi.org/10.1177/030098589603300506.
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To better define the histopathologic features of feline inflammatory liver disease, we studied feline liver biopsies evaluated at the University of Minnesota Veterinary Teaching Hospital over a 10-year period. Of 175 liver sections examined, 45 had portal inflammatory infiltrates. Of these, 60% had infiltrates consisting of lymphocytes and plasma cells, 24% had infiltrates consisting of neutrophils, and 16% had mixed infiltrates consisting of neutrophils, lymphocytes, and plasma cells. Lymphocytic-plasmacytic portal infiltrates were characterized by various degrees of bile duct proliferation and fibrosis without evidence of bile duct infiltration or periportal necrosis. Sections with portal neutrophilic infiltrates were characterized by bile duct infiltration, bile duct epithelial degeneration, periportal necrosis, and infiltration of neutrophils into adjacent lobules. We propose that hepatitis characterized by portal lymphocyte and plasma cell infiltration be termed lymphocytic portal hepatitis and that hepatitis characterized by cholangitis and portal neutrophilic infiltrates with or without lymphocytes and plasma cells be termed cholangiohepatitis.
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Li, Jianxu, Peng Guo, Masayuki Hirano, Brantley Herrin, and Max Cooper. "Cellular and molecular characterization of hagfish VLR-based adaptive immune system (VET2P.1043)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 207.15. http://dx.doi.org/10.4049/jimmunol.192.supp.207.15.
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Abstract Jawless vertebrates have an alternative adaptive immune system in which variable lymphocyte receptors (VLR) are somatically diversified through recombinatorial assembly of leucine-rich repeat cassettes during lymphocyte development. Three VLR loci (VLRA, VLRB, and VLRC) have been defined in lampreys and each is expressed by a distinct lymphocyte population. Lamprey VLRA and VLRC are expressed by T-like lineages of lymphocytes, whereas VLRB is expressed by a B-like lineage of lymphocytes, much like αβ T, γδ T and B cells in jawed vertebrates. Recently we have revised the nomenclature for the hagfish VLRs by defining a third VLR gene. Here, monoclonal and polyclonal antibodies were generated against invariant residues of hagfish VLRA, VLRB and VLRC and these were used to identify VLR-bearing lymphocytes and their products. We found that hagfish VLRA, VLRB and VLRC are expressed by three separate lymphocyte populations. Size-exclusion chromatography and western blot analysis indicated that multivalent VLRB proteins are released into the circulation, which suggests that hagfish VLRB+ cells are B-cell like. In contrast, neither VLRA nor VLRC was detectable in the plasma, supporting the hypothesis that these two lymphocyte populations are T-cell like. The demonstration of three lymphocyte populations in both lampreys and hagfish suggests that this tripartite lymphocytic differentiation program already existed in a common ancestor of the two cyclostome lineages around 480 Mya.
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Zhang, Jimin, Satish Devadas, and Yufang Shi. "Differential roles of CD95L and TRAIL in activation-induced cell death of cytotoxic T lymphocytes (110.22)." Journal of Immunology 188, no. 1_Supplement (May 1, 2012): 110.22. http://dx.doi.org/10.4049/jimmunol.188.supp.110.22.
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Abstract Cytotoxic T lymphocytes can be differentiated into type 1 (Tc1) and type 2 (Tc2) subsets as their T helper counterparts. Interestingly, our investigation in activation-induced cell death mechanisms reveals that CD95L mediates cell death in Tc1 lymphocytes and that Tc2 lymphocytes require TRAIL. Cell death in both subsets is also dependent on caspases. Inhibiting CD95L binding to its receptors in Tc1 lymphocytes from wild type mice displays altered Tc1 lymphocyte death, while Inhibiting TRAIL binding to its receptors in Tc2 lymphocytes shows altered Tc2 lymphocyte death. Activation-induced cell death in both Tc1 and Tc2 lymphocyte subsets can be blocked by pan caspase inhibitors. Moreover, Tc2 lymphocytes differentiated from TRAIL knockout mice show alleviated cell death. Rescued Tc2 lymphocytes secrete significantly higher amounts of IL-4, IL-5 and IL-10 while Tc1 lymphocytes produce higher IFN-γ and TNF-α. Our results indicate that CD95L and TRAIL play differential seminal roles in activation-induced cell death of these two cytotoxic T lymphocyte subsets, and that their different sensitivity to activation-induced cell death can alter CD8+ phenotype. With our study we conclude that Tc1 lymphocyte activation-induced cell death is mediated by CD95L while Tc2 lymphocytes undergo TRAIL-dependent activation-induced cell death.
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Karki, Shovana, Sansar Babu Tiwari, and Alina Basnet. "Evaluation of tumor infiltrating lymphocytes in breast carcinomas." Journal of Pathology of Nepal 12, no. 2 (September 30, 2022): 1909–12. http://dx.doi.org/10.3126/jpn.v12i2.47200.
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Background: Among the parameters that have a prognostic and/or predictive significance to therapeutic response, in the case of breast carcinoma, the study of tumor-infiltrating lymphocytes in breast carcinomas is emerging. The present study aimed to access the clinicopathological profiles of tumor-infiltrating lymphocytes in patients with primary breast carcinoma. Materials and Methods: Information was collected from the archive of the Department of Pathology, about invasive breast cancers diagnosed between April 2019 –March 2020. Hormone receptor status and Ki-67 index were assessed. For tumor-infiltrating lymphocytes, hematoxylin and eosin sections were evaluated following the guidelines of the “International Working Group for tumor-infiltrating lymphocytes in Breast Cancer—2014”. Results: High tumor-infiltrating lymphocytes were seen in 64.2% and 43.8% in ages < 50 and > 50 respectively. All cases of invasive lobular carcinoma had low tumor-infiltrating lymphocytes. 62.5% of T1 tumors were associated with low TILs whereas 80% of low tumor-infiltrating lymphocytes were T3. 71.4% of lymph node-positive tumors had low tumor-infiltrating lymphocytes. All breast cancers showed lymphocytic infiltrate. 40% of the tumors showed intermediate to high tumor-infiltrating lymphocytes. Lymphocyte-predominant breast cancers were 30%. Among the LPBC, 55.5% were triple-negative breast cancers, 33.3% were HR+, and 11.2% were HER2 positive. Conclusions: Low tumor-infiltrating lymphocytes presented at an advanced stage of the disease at the time of diagnosis. tumor-infiltrating lymphocytes in breasts decreased with increasing age. LPBCs were predominantly TNBCs. All breast cancers were immunogenic, stating the necessity to report tumor-infiltrating lymphocytes in all breast carcinomas.
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Juedes, Amy E., Evelyn Rodrigo, Lisa Togher, Laurie H. Glimcher, and Matthias G. von Herrath. "T-bet Controls Autoaggressive CD8 Lymphocyte Responses in Type 1 Diabetes." Journal of Experimental Medicine 199, no. 8 (April 19, 2004): 1153–62. http://dx.doi.org/10.1084/jem.20031873.
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The T-box transcription factor T-bet is known to control lineage commitment and interferon-γ production by T helper 1 (Th1) CD4 lymphocytes. We report here that T-bet is essential for development of CD8 lymphocyte-dependent autoimmune diabetes (type 1 diabetes [T1D]) in the rat insulin promoter–lymphocytic choriomeningitis virus (LCMV) transgenic model for virally induced T1D. In the absence of T-bet, autoaggressive (anti-LCMV) CD8 lymphocytes were reduced in number and produced less IFN-γ, but increased IL-2 compared with controls. Further analysis showed that T-bet intrinsically controls the generation, but not apoptosis, maintenance, or secondary expansion of antiviral effector/memory CD8 lymphocytes. This observation points toward a therapeutic opportunity for the treatment of T1D and other autoimmune disorders.
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Chu, Ming, Xiaobao Zhao, Lu Tang, Siwei Zhang, Shengkun Zhang, Dongdong Huang, Fuxiang Wang, and Lanlan Wei. "The correlation of lymphocytes with disease progression of COVID-19." Medicine 102, no. 48 (December 1, 2023): e36244. http://dx.doi.org/10.1097/md.0000000000036244.
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The aim of this study is to evaluate the potential of lymphocytes as biomarkers to predict the decline of coronavirus disease 2019 (COVID-19). Lymphocytes were counted in 164 moderate COVID-19 patients in Shenzhen, China. Among the moderate infected patients, 12.2% (20/164) progressed to severe cases after admission. Compared with the stable patients, the counts of lymphocytes, both total T lymphocytes and CD4+ T lymphocytes, in the severe patients, were lower. The aggravation of moderate infected patients was significantly associated with lymphocyte count (hazard ratio [HR] = 0.91; 95% confidence interval [CI]: 0.84–0.99), total T lymphocyte count (HR = 0.91; 95% CI: 0.84–0.99), and CD4+ T lymphocyte count (HR = 0.91; 95% CI: 0.85–0.98). Total T lymphocytes and CD4+ T lymphocytes could be important biomarkers to evaluate the risk of aggravation for moderate infected COVID-19 patients. The patients with low percentages of total T lymphocytes and CD4+ T lymphocytes need more attention.
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Todorović, Jasna, Marko Dinčić, Jelena Nešović Ostojić, Ivan Zaletel, Srdjan Lopičić, Duško Dundjerović, Svetislav Tatić, et al. "Differences in Chromatin Texture and Nuclear Fractal Dimension Between Hashimoto's and Lymphocytic Thyroiditis Lymphocytes." Microscopy and Microanalysis 25, no. 3 (February 28, 2019): 762–68. http://dx.doi.org/10.1017/s1431927619000163.
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AbstractPrevious evidence suggested that lymphocytic thyroiditis (LT) was a variant of Hashimoto's thyroiditis (HT), thus the aim of the current study is to quantify structural changes in histological specimens taken from HT and LT patients. A total of 600 images containing a single lymphocyte nucleus (300 nuclei per group) were obtained from 20 patients with HT and LT. In order to quantify changes in the nuclear architecture of investigated lymphocytes, the fractal dimension (FD) and some gray-level co-occurrence matrix texture parameters (angular second moment, inverse difference moment, contrast, entropy, and correlation) were calculated for each nucleus. A statistically significant difference in the FD of the “binary-outlined” nucleus and that of the corresponding “black-and-white” nucleus was detected between HT and LT lymphocyte nuclei. In addition, there was also a statistically significant difference in contrast and correlation between HT and LT lymphocyte nuclei. In conclusion, the results of this study suggested that there was a difference in structural complexity between investigated lymphocyte nuclei; additionally, LT lymphocytes possessed probably more complex texture and larger variations as well as more asymmetrical nuclei compared with HT lymphocytes. Accordingly, these findings indicate that LT is probably not a variant of HT; however, more complex studies are necessary to estimate differences between these types of thyroiditis.
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Lucivero, G., G. Pierucci, and L. Bonomo. "Lymphocyte subsets in peripheral blood and pleural fluid." European Respiratory Journal 1, no. 4 (April 1, 1988): 337–40. http://dx.doi.org/10.1183/09031936.93.01040337.
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We have examined the distribution of B and T lymphocytes, T-cells with helper/inducer (T4+) or suppressor/cytotoxic (T8+) phenotypes and a subset of cells with natural killer (NK) activity and positive for the Leu 7 (HNK-1) surface antigen in peripheral blood and in lymphocyte-rich pleural effusions of patients with tuberculosis or malignancies (mesothelioma and lung cancer with pleural metastasis). In individual patients, the percentages of T lymphocytes were uniformly higher in pleural effusions than in peripheral blood; however, lower percentages of B lymphocytes and cells positive for the Leu 7 antigen were present in pleural fluids. The analysis of T-cell subpopulations demonstrated a selective enrichment of T lymphocytes with helper/inducer phenotype in pleural effusions, while the percentages of T-cells with suppressor/cytotoxic phenotype were similar in pleural fluid and peripheral blood. These results indicate that in lymphocytic pleural effusions the main lymphoid cell population is represented by T lymphocytes with helper/inducer phenotype, regardless of whether the effusion is due to tuberculosis or malignancies such as mesothelioma or lung cancer.
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Avila, Monica, Bryan M. Fellman, and Russell Broaddus. "Tumor lymphocytic infiltration impacts recurrence in endometrioid-type endometrial carcinoma." Journal of Clinical Oncology 38, no. 15_suppl (May 20, 2020): e15239-e15239. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.e15239.
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e15239 Background: Endometrial cancers that have mismatch repair deficiency are associated with higher numbers of tumor-associated lymphocytes, but the clinical significance of this observation is unknown. Our objective was to quantify CD3+ and CD8+ tumor lymphocytes of MMR intact (MMRi) and MMRd endometrioid-type endometrial carcinomas and determine if there was an association with survival. Methods: MMRd was defined as endometrial carcinomas with loss of MLH1 expression due to MLH1 gene methylation and determined by immunohistochemistry. MMRi was defined as positive expression of MLH1, MSH2, MSH6, and PMS2. This was followed by Aperio image-based quantification was used to assess CD3+ and CD8+ lymphocyte populations in different regions of the primary endometrial carcinomas, including tumor periphery (tumor-myometrial interface), tumor center (bounded on all sides by tumor), and tumor hotspot (area with highest number of lymphocytes). Recurrence-free survival was estimated using Kaplan Meier and Cox regression. Median follow up time was 44 months. Results: 180 patients with endometrial carcinoma were analyzed of which 132 were MMRi and 48MMRd. The MMRd group had significantly higher levels of CD3+ and CD8+ lymphocytes regardless of which tumor region was assessed (Figure 1a, P < 0.001). Lymphocyte counts in both MMRd and MMRi groups had wide standard deviations such that there was some overlap in counts between the groups (Figure 1). Both MMRd and higher CD3+ counts were associated with worse recurrence-free survival. CD3+ quantification in the tumor periphery captured 21/23 recurrences (Figure 1b, HR = 8.04; 95% CI: 1.88 -34.31; p = 0.005); this included all of the MMRd cases that recurred and 7 MMRi cases with higher numbers of CD3+ lymphocytes that also recurred. Conclusions: MMRd endometrial cancers have increased numbers of CD3+ lymphocytic infiltrates within the primary tumor. Higher CD3+ infiltration is associated with greater risk of recurrence regardless of tumor location. In predicting tumor recurrence, lymphocytic counts performed better than assessment of MMR. Thus, quantification of CD3+ lymphocytes should be explored as a predictive biomarker.
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Gu, B. J., W. Y. Zhang, L. J. Bendall, I. P. Chessell, G. N. Buell, and J. S. Wiley. "Expression of P2X7purinoceptors on human lymphocytes and monocytes: evidence for nonfunctional P2X7receptors." American Journal of Physiology-Cell Physiology 279, no. 4 (October 1, 2000): C1189—C1197. http://dx.doi.org/10.1152/ajpcell.2000.279.4.c1189.
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Lymphocytes from normal subjects and patients with B-chronic lymphocytic leukemia (B-CLL) show functional responses to extracellular ATP characteristic of the P2X7receptor (previously termed P2Z). These responses include opening of a cation-selective channel/pore that allows entry of the fluorescent dye ethidium and activation of a membrane metalloprotease that sheds the adhesion molecule L-selectin. The surface expression of P2X7receptors was measured in normal leucocytes, platelets, and B-CLL lymphocytes and correlated with their functional responses. Monocytes showed four- to fivefold greater expression of P2X7than B, T, and NK lymphocytes, whereas P2X7expression on neutrophils and platelets was weak. All cell types demonstrated abundant intracellular expression of this receptor. All 12 subjects with B-CLL expressed lymphocyte P2X7at about the same level as B lymphocytes from normal subjects. P2X7function, measured by ATP-induced uptake of ethidium, correlated closely with surface expression of this receptor in normal and B-CLL lymphocytes and monocytes ( n = 47, r = 0.70; P< 0.0001). However, in three patients the ATP-induced uptake of ethidium into the malignant B lymphocytes was low or absent. The lack of P2X7function in these B lymphocytes was confirmed by the failure of ATP to induce Ba2+uptake into their lymphocytes. This lack of function of the P2X7receptor resulted in a failure of ATP-induced shedding of L-selectin, an adhesion molecule that directs the recirculation of lymphocytes from blood into the lymph node.
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Baadsgaard, O., D. A. Fox, and K. D. Cooper. "Human epidermal cells from ultraviolet light-exposed skin preferentially activate autoreactive CD4+2H4+ suppressor-inducer lymphocytes and CD8+ suppressor/cytotoxic lymphocytes." Journal of Immunology 140, no. 6 (March 15, 1988): 1738–44. http://dx.doi.org/10.4049/jimmunol.140.6.1738.
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Abstract In vivo exposure of human epidermis to UV abrogates the function of T6+DR+ Langerhans cells and induces the appearance of Ag-presenting T6-DR+ OKM5+ cells in the epidermis. Since UV exposure of murine skin results in Ts lymphocyte activation, we investigated the capacity of human epidermal cells (EC) harvested 3 days after in vivo UV exposure to activate regulatory and effector autologous T lymphocyte subsets. T lymphocytes were separated into CD8+ suppressor/cytotoxic lymphocytes and CD4+ helper/inducer lymphocytes by C lysis and panning. The CD4+ subset was further divided by using the 2H4 mAB to obtain CD4+2H4+ lymphocytes (inducers of TS lymphocytes) and CD4+2H4- lymphocytes (inducers of B cell Ig production and inducers of cytotoxic T cells). Unirradiated suction blister-derived EC from control skin (C-EC) and from skin exposed in vivo to UV (UV-EC) were cultured with purified autologous T lymphocyte subsets in the absence of added Ag. The resultant T lymphocyte proliferation was detected by [3H]thymidine uptake. UV-EC were highly effective in the stimulation of CD4+ lymphocytes, whereas C-EC were poor stimulators. The stimulator effect of UV-EC was abrogated after depletion of DR+ UV-EC. When CD4+ lymphocytes were fractionated, UV-EC consistently demonstrated enhanced ability to stimulate suppressor-inducer CD4+2H4+ lymphocytes relative to C-EC. Although less responsive than CD4+2H4+ lymphocytes, CD4+2H4- lymphocytes also demonstrated greater proliferation to UV-EC than to C-EC. Neither UV-EC nor C-EC were able to activate CD8+ lymphocytes devoid of CD4+ lymphocytes. However, after addition of rIL-2 at concentrations that allow binding only to the high affinity IL-2R on T lymphocytes, UV-EC induced vigorous proliferation of CD8+ lymphocytes, whereas C-EC induced only background levels of proliferation. C lysis of leukocytes resident within UV-EC resulted in 66 to 70% reduction of CD8+ lymphocyte proliferation. In conclusion, UV-EC may activate CD8+ lymphocytes by at least two pathways: (1) UV-EC activation of CD4+2H4+ lymphocytes may induce differentiation/proliferation of CD8+ suppressor cells and (2) UV-EC activation of CD4+ cells may induce IL-2 production, that, in combination with UV-induced epidermal leukocytes, stimulates CD8+ cells.
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McCutcheon, Ian E., and Edward H. Oldfield. "Lymphocytic adenohypophysitis presenting as infertility." Journal of Neurosurgery 74, no. 5 (May 1991): 821–26. http://dx.doi.org/10.3171/jns.1991.74.5.0821.
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✓ The authors report a nulliparous patient presenting with infertility and hyperprolactinemia. She underwent transsphenoidal surgery after radiological investigation disclosed an enlarged pituitary gland which did not respond to bromocriptine therapy. The removed tissue had histological features consistent with adenohypophysitis including a diffuse lymphocytic infiltrate. The lymphocyte subsets present in the infiltrate were characterized by immunohistochemical methods to establish the contribution of different elements of the cellular immune response. Lymphocytes bearing CD4 antigen (helper-inducer cells) were most prominent and appeared to bear the majority of the interleukin-2 receptor (expressed during lymphocytic activation) present in the pituitary gland. A few B lymphocytes were also observed. The location of the major histocompatibility antigen (classes I and II) and interleukin-2 receptor correlated with the lymphocytes and macrophages rather than with the stromal or parenchymal elements of the pituitary. Lymphocytic adenohypophysitis is an unusual cause of pituitary enlargement which can mimic a pituitary tumor, and is sometimes associated with hyperprolactinemia. In women of child-bearing age, it almost always occurs during pregnancy or the postpartum stage. The autoimmune disorder reported here has not previously been associated with infertility nor has the lymphocytic infiltrate of the pituitary previously been analyzed in detail by modern immunological methods.
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Maine, Christian J., John R. Teijaro, Kristi Marquardt, and Linda A. Sherman. "PTPN22 contributes to exhaustion of T lymphocytes during chronic viral infection." Proceedings of the National Academy of Sciences 113, no. 46 (October 31, 2016): E7231—E7239. http://dx.doi.org/10.1073/pnas.1603738113.
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The protein encoded by the autoimmune-associated protein tyrosine phosphatase nonreceptor type 22 gene,PTPN22, has wide-ranging effects in immune cells including suppression of T-cell receptor signaling and promoting efficient production of type I interferons (IFN-I) by myeloid cells. Here we show that mice deficient in PTPN22 resist chronic viral infection with lymphocytic choriomeningitis virus clone 13 (LCMV cl13). The numbers and function of viral-specific CD4 T lymphocytes is greatly enhanced, whereas expression of the IFNβ-induced IL-2 repressor, cAMP-responsive element modulator (CREM) is reduced. Reduction of CREM expression in wild-type CD4 T lymphocytes prevents the loss of IL-2 production by CD4 T lymphocytes during infection with LCMV cl13. These findings implicate the IFNβ/CREM/IL-2 axis in regulating T-lymphocyte function during chronic viral infection.
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Foa, R., M. Giovarelli, C. Jemma, MT Fierro, P. Lusso, ML Ferrando, F. Lauria, and G. Forni. "Interleukin 2 (IL 2) and interferon-gamma production by T lymphocytes from patients with B-chronic lymphocytic leukemia: evidence that normally released IL 2 is absorbed by the neoplastic B cell population." Blood 66, no. 3 (September 1, 1985): 614–19. http://dx.doi.org/10.1182/blood.v66.3.614.614.
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Abstract The capacity of T lymphocytes from patients with B cell chronic lymphocytic leukemia (B-CLL) to release interleukin 2 (IL 2) and interferon (IFN)-gamma was assessed following various stimuli. The spontaneous release of IL 2 and IFN-gamma was practically absent both with B-CLL and normal T lymphocytes. By contrast, after stimulation with phytohemagglutinin (PHA) or with PHA plus 12-O- tetradecanoylphorbol-13-acetate, the production of IL 2 and IFN-gamma by B-CLL T lymphocytes was similar to that of normal T lymphocytes, irrespective of the reversed T lymphocyte subset distribution (OKT4/OKT8 ratio) observed in B-CLL. However, the titer of IL 2 was greatly reduced when autologous leukemic B cells were added to the culture system. Unlike IL 2, the presence of leukemic B cells did not affect the titer of IFN-gamma in the culture supernatants. The indication that IL 2 may be adsorbed in vivo by the neoplastic B cells was further confirmed by the demonstration of the IL 2 receptor (revealed by anti-Tac monoclonal antibody) on the leukemic B cells, particularly following mitogenic stimulation, and by the evidence that exogenous IL 2 can be directly absorbed by untreated B-CLL T lymphocytes to release IFN-gamma and IL 2 is preserved, but that IL 2 may be rapidly removed by the neoplastic B-CLL cells, thus contributing to the well-documented T lymphocyte abnormalities present in this disease.
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Foa, R., M. Giovarelli, C. Jemma, MT Fierro, P. Lusso, ML Ferrando, F. Lauria, and G. Forni. "Interleukin 2 (IL 2) and interferon-gamma production by T lymphocytes from patients with B-chronic lymphocytic leukemia: evidence that normally released IL 2 is absorbed by the neoplastic B cell population." Blood 66, no. 3 (September 1, 1985): 614–19. http://dx.doi.org/10.1182/blood.v66.3.614.bloodjournal663614.
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The capacity of T lymphocytes from patients with B cell chronic lymphocytic leukemia (B-CLL) to release interleukin 2 (IL 2) and interferon (IFN)-gamma was assessed following various stimuli. The spontaneous release of IL 2 and IFN-gamma was practically absent both with B-CLL and normal T lymphocytes. By contrast, after stimulation with phytohemagglutinin (PHA) or with PHA plus 12-O- tetradecanoylphorbol-13-acetate, the production of IL 2 and IFN-gamma by B-CLL T lymphocytes was similar to that of normal T lymphocytes, irrespective of the reversed T lymphocyte subset distribution (OKT4/OKT8 ratio) observed in B-CLL. However, the titer of IL 2 was greatly reduced when autologous leukemic B cells were added to the culture system. Unlike IL 2, the presence of leukemic B cells did not affect the titer of IFN-gamma in the culture supernatants. The indication that IL 2 may be adsorbed in vivo by the neoplastic B cells was further confirmed by the demonstration of the IL 2 receptor (revealed by anti-Tac monoclonal antibody) on the leukemic B cells, particularly following mitogenic stimulation, and by the evidence that exogenous IL 2 can be directly absorbed by untreated B-CLL T lymphocytes to release IFN-gamma and IL 2 is preserved, but that IL 2 may be rapidly removed by the neoplastic B-CLL cells, thus contributing to the well-documented T lymphocyte abnormalities present in this disease.
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Link, DC, and M. Zutter. "The proto-oncogene c-fgr is expressed in normal mantle zone B lymphocytes and is developmentally regulated during myelomonocytic differentiation in vivo." Blood 85, no. 2 (January 15, 1995): 472–79. http://dx.doi.org/10.1182/blood.v85.2.472.472.
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Abstract The proto-oncogene c-fgr is a member of the c-src gene family of cytoplasmic tyrosine kinases. Previous studies have suggested that it is normally expressed in neutrophils, monocytes, macrophages, and natural killer cells. c-fgr is also expressed in the B cells of certain lymphoproliferative disorders, namely, Epstein-Barr virus-associated lymphoproliferative disease, and in chronic lymphocytic leukemia, but it has not previously been detected in normal or reactive human lymphoid tissue. In this study we have determined the pattern of p55c- fgr protein expression in normal human hematopoietic and lymphoid tissues at the single-cell level using immunohistochemical and immunofluorescent techniques. We show that p55c-fgr expression is developmentally regulated with high-level expression first evident at the myelocyte stage of myeloid differentiation. In addition, we show that p55c-fgr is expressed in circulating B lymphocytes isolated from chronic lymphocytic leukemia patients but is not expressed in normal circulating B lymphocytes. Surprisingly, p55c-fgr is also expressed in a subpopulation of normal B lymphocytes, the mantle zone B lymphocytes. This demonstration that p55c-fgr is expressed in a normal B-lymphocyte subpopulation suggests that its expression in certain B-cell lymphoproliferative disorders may be an indirect consequence of, rather than a primary cause of, the neoplastic transformation process.
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Link, DC, and M. Zutter. "The proto-oncogene c-fgr is expressed in normal mantle zone B lymphocytes and is developmentally regulated during myelomonocytic differentiation in vivo." Blood 85, no. 2 (January 15, 1995): 472–79. http://dx.doi.org/10.1182/blood.v85.2.472.bloodjournal852472.
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The proto-oncogene c-fgr is a member of the c-src gene family of cytoplasmic tyrosine kinases. Previous studies have suggested that it is normally expressed in neutrophils, monocytes, macrophages, and natural killer cells. c-fgr is also expressed in the B cells of certain lymphoproliferative disorders, namely, Epstein-Barr virus-associated lymphoproliferative disease, and in chronic lymphocytic leukemia, but it has not previously been detected in normal or reactive human lymphoid tissue. In this study we have determined the pattern of p55c- fgr protein expression in normal human hematopoietic and lymphoid tissues at the single-cell level using immunohistochemical and immunofluorescent techniques. We show that p55c-fgr expression is developmentally regulated with high-level expression first evident at the myelocyte stage of myeloid differentiation. In addition, we show that p55c-fgr is expressed in circulating B lymphocytes isolated from chronic lymphocytic leukemia patients but is not expressed in normal circulating B lymphocytes. Surprisingly, p55c-fgr is also expressed in a subpopulation of normal B lymphocytes, the mantle zone B lymphocytes. This demonstration that p55c-fgr is expressed in a normal B-lymphocyte subpopulation suggests that its expression in certain B-cell lymphoproliferative disorders may be an indirect consequence of, rather than a primary cause of, the neoplastic transformation process.
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Kurashige, Takashi, Tomomi Murao, Naoko Mine, Tomohito Sugiura, Yukiko Inazuka, Kazuya Kuraoka, Tetsuya Takahashi, Hirofumi Maruyama, and Tsuyoshi Torii. "Anti-HMGCR Antibody-Positive Myopathy Shows Bcl-2-Positive Inflammation and Lymphocytic Accumulations." Journal of Neuropathology & Experimental Neurology 79, no. 4 (February 25, 2020): 448–57. http://dx.doi.org/10.1093/jnen/nlaa006.
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Abstract Anti-3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR) and antisignal recognition particle (SRP) antibodies are frequently associated with immune-mediated necrotizing myopathy (IMNM). However, the difference in clinical manifestations between anti-HMGCR and anti-SRP antibodies is unclear. HMGCR is an essential enzyme for cholesterol biosynthesis and is inhibited by statins that regulate apoptosis of Bcl-2-positive and beta chemokine receptor 4 (CCR4)-positive lymphoma cells. In this study, we aimed to clarify Bcl-2 and CCR4 expressions of lymphocytes in anti-HMGCR antibody-positive IMNM and explore the difference between anti-HMGCR antibody-positive myopathy and other inflammatory myopathies. We retrospectively examined Bcl-2- and CCR4-positive lymphocyte infiltrations in muscle and skin biopsy specimens from 19 anti-HMGCR antibody-positive patients and 75 other idiopathic inflammatory myopathies (IIMs) patients. A higher incidence of Bcl-2- and CCR4-positive lymphocytes was detected in the muscle and skin of anti-HMGCR antibody-positive IMNM patients (p < 0.001). In 5 patients with anti-HMGCR antibodies, Bcl-2-positive lymphocytes formed lymphocytic accumulations, which were not observed in other IIMs. Low-density lipoprotein cholesterol levels were not increased except for patients with Bcl-2-positive lymphocytic accumulations (p = 0.010). Bcl-2 and CCR4 lymphocyte infiltrations could be a pathological characteristic of anti-HMGCR antibody-positive IMNM.
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Park, Suk W., Walter Royal, Richard D. Semba, Gordon W. Wiegand, and Diane E. Griffin. "Expression of Adhesion Molecules and CD28 on T Lymphocytes during Human Immunodeficiency Virus Infection." Clinical Diagnostic Laboratory Immunology 5, no. 4 (July 1, 1998): 583–87. http://dx.doi.org/10.1128/cdli.5.4.583-587.1998.
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ABSTRACT Adhesion molecules, which play a major role in lymphocyte circulation, have not been well characterized in human immunodeficiency virus (HIV) infection. T-lymphocyte populations, including CD3, CD4, CD28, and adhesion molecules (L selectin, LFA-1, VLA-4, and ICAM-1) were measured by flow cytometry in a cross-sectional study of 100 HIV-infected and 49 HIV-seronegative adults. HIV-infected adults had lower numbers of CD3+ lymphocytes expressing L selectin (P < 0.0001) and VLA-4 (P < 0.01) and higher numbers of CD3+ lymphocytes expressing LFA-1bright (P < 0.002) than did HIV-negative adults. By CD4+-lymphocyte count category (>500, 200 to 500, or <200 cells/μl), HIV-infected adults with more advanced disease had lower percentages of CD3+ lymphocytes expressing L selectin and VLA-4 and higher percentages of CD3+ lymphocytes expressing LFA-1. The percentages of CD3+ CD28+ lymphocytes and of CD3+L selectin+ lymphocytes were positively correlated (Spearman coefficient = 0.86; P < 0.0001), and the percentage of CD3+ CD28+ lymphocytes and the CD3+ LFA-1bright lymphocyte/CD3+LFA-1dim lymphocyte ratio were negatively correlated (Spearman coefficient = −0.92; P <0.00001). The results of this study suggest that HIV infection is associated with altered expression of adhesion molecules.
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Peng, Cong, Zongwei Guo, Yue Zhao, Rui Li, Liang Wang, and Wenping Gong. "Effect of Lymphocyte Subsets on Bone Density in Senile Osteoporosis: A Retrospective Study." Journal of Immunology Research 2022 (October 26, 2022): 1–11. http://dx.doi.org/10.1155/2022/3337622.
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Background. Several studies have shown that lymphocyte subsets can mediate the occurrence of osteoporosis (OP); however, the predictive ability of lymphocyte subsets in senile OP has not been elucidated. Purpose. To investigate the ability of lymphocyte subsets to predict senile osteoporosis (OP). Methods and Materials. This study included 44 patients with senile OP and 44 without OP. Dual-energy X-ray absorptiometry (DEXA) was used to determine bone mineral density (BMD). Flow cytometry was used to analyze the absolute counts of the lymphocyte subsets and cytokine levels. Finally, the correlation between BMD and lymphocyte subset counts in the two groups was analyzed. Results. There were no significant differences in age, sex, or weight between the OP and non-OP groups. The absolute counts of total T lymphocytes and CD8+ T lymphocytes in the OP group were significantly lower than those in the non-OP group. The levels of IFN-γ or TNF-α in the OP group were significantly higher or lower, respectively, than those in the non-OP group. PCA showed that age, BMI, total T lymphocytes, CD4+ T lymphocytes, CD8+ T lymphocytes, and B lymphocytes were the principal components of senile OP. The linear regression equation showed that BMD of the right femoral neck significantly decreased with a decline in CD8+ T lymphocyte counts. Conclusion. BMD decreased with a decrease in CD8+ T lymphocytes. The mechanism by which lower lymphocyte subsets lead to lower BMD may be related to abnormal bone metabolism caused by immune aging. Therefore, we considered that CD8+ T lymphocytes could be used to predict the incidence of senile OP.
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Mohr, Audrey, Yves Renaudineau, Jacques-Olivier Pers, Christophe Jamin, and Anne Bordron. "B lymphocytes of chronic lymphocytic leukemia, regulatory B lymphocytes which ignore?" Hématologie 22, no. 1 (January 2016): 22–28. http://dx.doi.org/10.1684/hma.2016.1083.
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Loffredo, John T., Eva G. Rakasz, Juan Pablo Giraldo, Sean P. Spencer, Kelly K. Grafton, Sarah R. Martin, Gnankang Napoé, Levi J. Yant, Nancy A. Wilson, and David I. Watkins. "Tat28-35SL8-Specific CD8+ T Lymphocytes Are More Effective than Gag181-189CM9-Specific CD8+ T Lymphocytes at Suppressing Simian Immunodeficiency Virus Replication in a Functional In Vitro Assay." Journal of Virology 79, no. 23 (December 15, 2005): 14986–91. http://dx.doi.org/10.1128/jvi.79.23.14986-14991.2005.
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ABSTRACT Epitope-specific CD8+ T lymphocytes may play an important role in controlling human immunodeficiency virus (HIV)/simian immunodeficiency virus replication. Unfortunately, standard cellular assays do not measure the antiviral efficacy (the ability to suppress virus replication) of CD8+ T lymphocytes. Certain epitope-specific CD8+ T lymphocytes may be better than others at suppressing viral replication. We compared the antiviral efficacy of two immunodominant CD8+ T lymphocyte responses—Tat28-35SL8 and Gag181-189CM9—by using a functional in vitro assay. Viral suppression by Tat-specific CD8+ T lymphocytes was consistently greater than that of Gag-specific CD8+ T lymphocytes. Such differences in antigen-specific CD8+-T-lymphocyte efficacy may be important for selecting CD8+ T lymphocyte epitopes for inclusion in future HIV vaccines.
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Tan, J., B. Deleuran, B. Gesser, H. Maare, M. Deleuran, C. G. Larsen, and K. Thestrup-Pedersen. "Regulation of human T lymphocyte chemotaxis in vitro by T cell-derived cytokines IL-2, IFN-gamma, IL-4, IL-10, and IL-13." Journal of Immunology 154, no. 8 (April 15, 1995): 3742–52. http://dx.doi.org/10.4049/jimmunol.154.8.3742.
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Abstract There has been a number of conflicting reports regarding the T lymphocyte chemotactic activities of several cytokines. IL-2 and IFN-gamma are known to promote augmentation of immune inflammation, whereas IL-4, IL-10, and IL-13 display immunomodulatory effects on inflammatory cells including inhibition of cytokine production. Their effects on chemotaxis of inflammatory cells are unknown. We observed that IL-1 alpha could induce chemotaxis both in overnight cultured and anti-CD3 mAb-activated T lymphocytes and that overnight culture and anti-CD3 activation increase the number of IL-1R on T lymphocytes. In contrast, IL-8 selectively attracts freshly isolated T lymphocytes. Staurosporine inhibits freshly isolated T lymphocyte chemotaxis toward IL-8, whereas tyrphostin 23 inhibits chemotaxis of overnight cultured and anti-CD3-activated T lymphocytes toward IL-1 alpha. We have found that IL-2 and IL-13 inhibit the chemotactic migration of both CD4+ and CD8+ T lymphocytes toward IL-8, and RANTES. IL-4 inhibits only CD8+ T lymphocyte chemotaxis toward RANTES, IL-8 and IL-10. IL-10 inhibits only CD4+ T lymphocytes in their chemotactic response toward RANTES and IL-8. IFN-gamma does on the other hand augment the sensitivity of human T lymphocytes to chemotactic stimuli. Thus, our results demonstrate that different proinflammatory cytokines will induce chemotactic migration of T lymphocytes under different circumstances acting through different signaling pathways. The T cell-derived cytokines IL-2, IL-4, IL-10, and IL-13 are able to block further T lymphocyte chemotaxis, thus leading to a focusing of T lymphocytes in an area of T lymphocyte activation. These mechanisms seem relevant in our understanding of the specific and continuous localization of T lymphocytes in allergic and autoimmune disorders.
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Steeber, D. A., N. E. Green, S. Sato, and T. F. Tedder. "Lyphocyte migration in L-selectin-deficient mice. Altered subset migration and aging of the immune system." Journal of Immunology 157, no. 3 (August 1, 1996): 1096–106. http://dx.doi.org/10.4049/jimmunol.157.3.1096.
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Abstract Lymphocyte trafficking across high endothelial venules (HEV) of peripheral lymph nodes (PLN) is dependent upon lymphocyte expression of L-selectin. Mice that lack this adhesion molecule provide an opportunity to determine the long-term role of L-selectin-mediated migration in the maintenance of leukocyte subpopulations. HEV in L-selectin-deficient mice were phenotypically, morphologically, and functionally comparable with wild-type mice, although there was a 70 to 90% reduction in the number of lymphocytes within PLN. These lymphocytes most likely entered PLN through the afferent lymphatics, since they did not migrate into PLN of normal mice during short-term homing experiments. The impaired trafficking of lymphocytes across PLN-HEV resulted in the accumulation of memory (CD18highCD44high) lymphocytes within PLN, and also altered the distribution of lymphocyte subpopulations within other tissues. Specifically, a 30 to 55% increase in splenic cellularity occurred due to increases in both naive and memory lymphocytes. Circulating lymphocyte numbers or subpopulations were not altered in young L-selectin-deficient mice, but circulating monocyte numbers were increased nearly threefold. In contrast, older L-selectin-deficient mice had disproportionate increases of both naive and memory CD4+ T cells present within spleen and blood. These results and the finding that memory lymphocytes in wild-type mice expressed L-selectin demonstrate a requirement for L-selectin in the regulation of memory lymphocyte migration. Therefore, L-selectin-dependent pathways of lymphocyte migration are important for the normal migration of both naive and memory lymphocytes.
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Broström, Hans, Marita Troye-Bomberg, and Peter Perlmann. "Generation of in vitro natural cytotoxicity of horse lymphocytes against sarcoid-derived tumor cells not expressing major histocompatibility complex antigens." American Journal of Veterinary Research 57, no. 7 (July 1, 1996): 992–99. http://dx.doi.org/10.2460/ajvr.1996.57.07.992.
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Abstract Objective To analyze in vitro lymphocyte-mediated immune responses of horses with sarcoids against allogeneic sarcoid cells containing endogenous retrovirus but not expressing major histocompatibility complex antigens. Design Lymphocyte-mediated immune reactions were assessed by means of proliferative responses in mixed lymphocyte tumor cell culture (MLTC) assay and lymphocyte-mediated cytotoxicity against various equine target cells. Animals 12 horses with sarcoid tumors and 15 control horses. Procedure Blood lymphocytes were cocultured in MLTC with allogeneic sarcoid cells (Mc-1, BayMc-1), equine testis cells, or normal equine dermal fibroblasts. Lymphocytes were assayed for proliferative responses by [3H]thymidine uptake and for cytotoxicity against the same targets by 51Cr release assay. The lymphocyte populations were analyzed for some common surface markers. Results Lymphocytes from horses with sarcoids exerted an anamnestic proliferative response in MLTC against Mc-1 cells, but this procedure never generated cytotoxic lymphocytes. However, lymphocytes from all horses cultured in medium with 10% allogeneic serum only had selective, natural cytotoxicity against Mc-1 that was generated without DNA synthesis. Approximately 80% of the lymphocytes disappeared during culture; however the remaining population of small, viable lymphocytes indicated a decrease of CD4+ and CD8+ T lymphocytes, but numbers of T cells with receptors for Helix pomatia A hemagglutinin were unaffected. Few lymphocytes had Fc-receptors for IgG, were complement-reactive positive cells, or were B cells expressing surface immunoglobulin. Conclusions Results may indicate a natural defense system, which preferentially recognizes and lyses tumor cells that are deficient in surface expression of major histocompatibility complex antigens, without intervention of conventional T-cell receptors or antibodies. (Am J Vet Res 1996;57:992–999)
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Mathur, A., D. H. Conrad, and R. G. Lynch. "Characterization of the murine T cell receptor for IgE (Fc epsilon RII). Demonstration of shared and unshared epitopes with the B cell Fc epsilon RII." Journal of Immunology 141, no. 8 (October 15, 1988): 2661–67. http://dx.doi.org/10.4049/jimmunol.141.8.2661.
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Abstract Antigenic relationships between the low affinity Fc epsilon R present on murine B and T lymphocytes were studied. A rat mAb (B3B4) and two polyclonal antisera produced by immunizing with the murine B lymphocyte Fc epsilon RII were examined for their ability to inhibit binding of IgE to murine B or T lymphocytes, using an IgE-specific rosette assay. One polyclonal antiserum (goat-anti-mouse Fc epsilon R) inhibited binding of IgE to both B and T lymphocytes, whereas another polyclonal antiserum (rabbit-anti-mouse Fc epsilon R) and the rat mAb inhibited the binding of IgE to B lymphocytes but did not influence the binding of IgE to T lymphocytes. When lymphocytes were surface labeled with 125I, 49-kDa and 38-kDa IgE-binding proteins were immunoprecipitated from B lymphocyte lysates by B3B4 and from B and T lymphocyte lysates by the goat antiserum. Taken together, these results suggest that the Fc epsilon R present on murine B and T lymphocytes are structurally related receptors that share some, but not all, epitopes.
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Issekutz, T. B. "Effects of six different cytokines on lymphocyte adherence to microvascular endothelium and in vivo lymphocyte migration in the rat." Journal of Immunology 144, no. 6 (March 15, 1990): 2140–46. http://dx.doi.org/10.4049/jimmunol.144.6.2140.
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Abstract The first step in the migration of lymphocytes out of the blood is adherence of lymphocytes to endothelial cells (EC) in the postcapillary venule. It is thought that in inflammatory reactions cytokines activate the endothelium to promote lymphocyte adherence and migration into the inflammatory site. Injection of IFN-gamma, IFN-alpha/beta, and TNF-alpha into the skin of rats stimulated the migration of small peritoneal exudate lymphocytes (sPEL) into the injection site, and these cytokines mediated lymphocyte recruitment to delayed-type hypersensitivity, sites of virus injection, and in part to LPS. The effect of cytokines on lymphocyte adherence to rat microvascular EC was examined. IFN-gamma, IFN-alpha/beta, IL-1, TNF-alpha, and TNF-beta increased the binding of small peritoneal exudate lymphocyte (sPEL) to EC. IFN-gamma was more effective and stimulated adherence at much lower concentrations than the other cytokines. IL-2 did not increase lymphocyte adherence. LPS strongly stimulated lymphocyte binding. Treatment of EC, but not sPEL, enhanced adhesion, and 24 h of treatment with IFN-gamma and IL-1 induced near maximal adhesion. Lymph node lymphocytes, which migrate poorly to inflammatory sites, adhered poorly to unstimulated and stimulated EC, whereas sPEL demonstrated significant spontaneous adhesion which was markedly increased by IFN-gamma, IL-1, and LPS. Spleen lymphocytes showed an intermediate pattern of adherence. Combinations of IFN-gamma and TNF-alpha were additive in stimulating sPEL-EC adhesion. Depletion of sPEL and spleen T cells by adherence to IFN-gamma stimulated EC decreased the in vivo migration of the lymphocytes to skin sites injected with IFN-gamma, IFN-alpha/beta, TNF-alpha, poly I:C, LPS, and to delayed-type hypersensitivity reactions by 50%, and significantly increased the migration of these cells to normal lymph nodes, as compared to unfractionated lymphocytes. Thus the cytokines and lymphocytes involved in migration to cutaneous inflammation in the rat stimulate lymphocyte adhesion to rat EC in vitro, and IFN-gamma stimulated EC appear to promote the selective adhesion of inflammatory site-seeking lymphocytes.
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Tolstykh, E. I., M. O. Degteva, and A. V. Akleyev. "Estimation of lymphocyte radiation doses after the ingestion of radionuclides of different tropicity." Radiatsionnaya Gygiena = Radiation Hygiene 14, no. 3 (October 9, 2021): 18–28. http://dx.doi.org/10.21514/1998-426x-2021-14-3-18-28.
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Assessment of the lymphocyte doses is relevant for solving a number of radiobiological problems, including the risk assessment of hemoblastosis (leukemia, multiple myeloma, lymphoma etc.), as well as the use of circulating lymphocytes as “natural biodosimeters”. The latter is because the frequency of chromosomal aberrations occurring in lymphocytes following radiation exposure is proportional to the accumulated dose. Assessment of doses to the circulating lymphocytes requires due account of: first, the dose accumulated by the lymphocyte progenitors in the red bone marrow; and second, the dose accumulated during lymphocyte circulation through lymphoid organs. The models presented by International Commission on Radiological Protection (ICRP-67, ICRP-100) allow calculating the dose for specific lymphoid organs based on known level of radionuclide intakes. A recently developed model of circulating T-lymphocyte irradiation takes into account all sources of exposure and age-related dynamics of T-lymphocytes: (1) exposure of lymphocyte progenitors in red bone marrow: (2) exposure of T-lymphocytes in the lymphoid organs, taking into account the proportion of resident lymphocytes and the residence time of circulating lymphocytes in the specific lymphoid organs. The objective of the study is to assess the dose coefficients allowing for the transition from the ingestion of 141,144Ce, 95Zr, 103,106Ru, 95Nb to the doses accumulated in circulating T-lymphocytes. For calculations, we used the dose coefficients from ICRP publications for specific lymphoid organs, as well as published data on the residence time of circulating lymphocytes in lymphoid organs and tissues. As a result, it was shown that the doses in circulating T-lymphocytes are higher than those in the red bone marrow, but lower than the doses to the colon wall. The dose coefficients were age dependent; the maximum values were typical for newborns. The obtained dose coefficients for 141,144Ce, 95Zr, 95Nb and 103,106Ru can be used to estimate the tissue and organ doses based on data on the frequency of chromosomal aberrations in peripheral blood lymphocytes.
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Froom, P., B. Ramot, M. Biniaminov, and D. Douer. "Production of burst-promoting activity by monoclonal antibody defined malignant T lymphocytes from patients with lymphocytic leukemia and lymphoma." Blood 65, no. 4 (April 1, 1985): 997–1001. http://dx.doi.org/10.1182/blood.v65.4.997.997.
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Abstract We tested conditioned media from 12 patients with T lymphocyte neoplasms and four T cell lines for their ability to stimulate the in vitro growth of erythroid-burst-forming units (BFU-E) from bone marrow mononuclear cells in a methylcellulose culture system. Nine patients suffered from acute lymphocytic leukemia, two from chronic lymphocytic leukemia, and one from non-Hodgkin's lymphoma. The T lymphocytes were characterized by a series of monoclonal antibodies and their stage of development was correlated with their ability to produce burst- promoting activity (BPA). Conditioned media from cells classified as prothymocytes (three cases), common thymocytes (one case), mature thymocytes (three cases), and mature lymphocytes of the helper subtype (two cases) increased BFU-E proliferation four- to 19-fold over control values using normal bone marrow as target cells. Conditioned media from OKT8+ malignant T lymphocytes (three cases) did not enhance BFU-E proliferation. Conditioned media from cells classified as immature T cells stimulated CFU-GM proliferation in only one of seven cases even though they secreted BPA. Conditioned media from three of the four cell lines stimulated by phytohemagglutinin, enhanced BFU-E growth. Our results indicate that malignant cells that have characteristics of immature T cells are able to produce BPA. Studies using techniques to isolate homogeneous populations of normal T cell subsets are required to determine whether normal immature T lymphocytes have the same capability.
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Froom, P., B. Ramot, M. Biniaminov, and D. Douer. "Production of burst-promoting activity by monoclonal antibody defined malignant T lymphocytes from patients with lymphocytic leukemia and lymphoma." Blood 65, no. 4 (April 1, 1985): 997–1001. http://dx.doi.org/10.1182/blood.v65.4.997.bloodjournal654997.
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We tested conditioned media from 12 patients with T lymphocyte neoplasms and four T cell lines for their ability to stimulate the in vitro growth of erythroid-burst-forming units (BFU-E) from bone marrow mononuclear cells in a methylcellulose culture system. Nine patients suffered from acute lymphocytic leukemia, two from chronic lymphocytic leukemia, and one from non-Hodgkin's lymphoma. The T lymphocytes were characterized by a series of monoclonal antibodies and their stage of development was correlated with their ability to produce burst- promoting activity (BPA). Conditioned media from cells classified as prothymocytes (three cases), common thymocytes (one case), mature thymocytes (three cases), and mature lymphocytes of the helper subtype (two cases) increased BFU-E proliferation four- to 19-fold over control values using normal bone marrow as target cells. Conditioned media from OKT8+ malignant T lymphocytes (three cases) did not enhance BFU-E proliferation. Conditioned media from cells classified as immature T cells stimulated CFU-GM proliferation in only one of seven cases even though they secreted BPA. Conditioned media from three of the four cell lines stimulated by phytohemagglutinin, enhanced BFU-E growth. Our results indicate that malignant cells that have characteristics of immature T cells are able to produce BPA. Studies using techniques to isolate homogeneous populations of normal T cell subsets are required to determine whether normal immature T lymphocytes have the same capability.
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Consoli, Ugo, Iman El-Tounsi, Alex Sandoval, Virginia Snell, Hans-Dieter Kleine, Wendy Brown, Johnnie R. Robinson, Francesco DiRaimondo, William Plunkett, and Michael Andreeff. "Differential Induction of Apoptosis by Fludarabine Monophosphate in Leukemic B and Normal T Cells in Chronic Lymphocytic Leukemia." Blood 91, no. 5 (March 1, 1998): 1742–48. http://dx.doi.org/10.1182/blood.v91.5.1742.
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Abstract Fludarabine (F-ara-A), an adenine nucleoside analog with efficacy in B-cell chronic lymphocytic leukemia (B-CLL), has also been shown to have a long-lasting suppressive effect on T lymphocytes. In heterogeneous clinical samples, apoptosis cannot be detected by standard methods in small cellular subsets. We developed, therefore, a combined assay of in situ end-labeling of nicked DNA by terminal deoxynucleotide transferase, with measurements of cellular DNA content and surface antigens (CD3, CD4, CD8, and CD19) by multiparametric flow cytometry. This assay was used to determine F-ara-A–induced apoptosis in different lymphocyte subsets from CLL patients and normal controls treated with F-ara-A in vitro. Apoptosis was also correlated to bcl-2 protein levels. We observed a direct effect of F-ara-A on both B-CLL and T lymphocytes. The response to F-ara-A in B-CLL lymphocytes in vitro was Rai stage–dependent, the early-stages being more responsive (P = .01). Higher levels of spontaneous apoptosis were observed in B-CLL lymphocytes from early stage patients (P = .02). No difference was observed in spontaneous apoptosis of normal T cells in B-CLL, although T lymphocytes in late-stage disease were more sensitive to F-ara-A–induced apoptosis. Incubation with cyclosporin A did not affect B-CLL and T-lymphocyte survival compared with control cultures. Results suggested a direct apoptotic effect of F-ara-A on B-CLL lymphocytes that decreases with increasing clinical stage. No correlation was found between bcl-2 and spontaneous or F-ara-A–induced apoptosis. Apoptosis occurred at all cell-cycle stages and was not restricted to cells in S phase. The mechanisms of this stage-dependent apoptosis in CLL remain to be elucidated.
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Consoli, Ugo, Iman El-Tounsi, Alex Sandoval, Virginia Snell, Hans-Dieter Kleine, Wendy Brown, Johnnie R. Robinson, Francesco DiRaimondo, William Plunkett, and Michael Andreeff. "Differential Induction of Apoptosis by Fludarabine Monophosphate in Leukemic B and Normal T Cells in Chronic Lymphocytic Leukemia." Blood 91, no. 5 (March 1, 1998): 1742–48. http://dx.doi.org/10.1182/blood.v91.5.1742.1742_1742_1748.
Full textAbstract:
Fludarabine (F-ara-A), an adenine nucleoside analog with efficacy in B-cell chronic lymphocytic leukemia (B-CLL), has also been shown to have a long-lasting suppressive effect on T lymphocytes. In heterogeneous clinical samples, apoptosis cannot be detected by standard methods in small cellular subsets. We developed, therefore, a combined assay of in situ end-labeling of nicked DNA by terminal deoxynucleotide transferase, with measurements of cellular DNA content and surface antigens (CD3, CD4, CD8, and CD19) by multiparametric flow cytometry. This assay was used to determine F-ara-A–induced apoptosis in different lymphocyte subsets from CLL patients and normal controls treated with F-ara-A in vitro. Apoptosis was also correlated to bcl-2 protein levels. We observed a direct effect of F-ara-A on both B-CLL and T lymphocytes. The response to F-ara-A in B-CLL lymphocytes in vitro was Rai stage–dependent, the early-stages being more responsive (P = .01). Higher levels of spontaneous apoptosis were observed in B-CLL lymphocytes from early stage patients (P = .02). No difference was observed in spontaneous apoptosis of normal T cells in B-CLL, although T lymphocytes in late-stage disease were more sensitive to F-ara-A–induced apoptosis. Incubation with cyclosporin A did not affect B-CLL and T-lymphocyte survival compared with control cultures. Results suggested a direct apoptotic effect of F-ara-A on B-CLL lymphocytes that decreases with increasing clinical stage. No correlation was found between bcl-2 and spontaneous or F-ara-A–induced apoptosis. Apoptosis occurred at all cell-cycle stages and was not restricted to cells in S phase. The mechanisms of this stage-dependent apoptosis in CLL remain to be elucidated.
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Kenney, D., L. Cairns, E. Remold-O'Donnell, J. Peterson, FS Rosen, and R. Parkman. "Morphological abnormalities in the lymphocytes of patients with the Wiskott-Aldrich syndrome." Blood 68, no. 6 (December 1, 1986): 1329–32. http://dx.doi.org/10.1182/blood.v68.6.1329.1329.
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Abstract Lymphocytes from 18 patients with the Wiskott-Aldrich Syndrome (WAS) were examined by scanning electron microscopy (SEM). Most peripheral blood lymphocytes from normal individuals are covered with slender microvillus projections, but a large proportion of lymphocytes from WAS patients were found to be relatively devoid of microvilli. A lymphocyte morphology scoring system was developed to quantify the density of microvilli: Grade 4 classified those lymphocytes with greater than 75% of the surface covered with microvilli with progressive decrements to grade 1, which were those without microvilli. The mean lymphocyte morphology score of eight normal individuals was 3.62 +/- .22. The mean lymphocyte score of WAS patients was substantially lower (2.89 +/- .27, P less than .001). In addition, WAS lymphocytes often were qualitatively abnormal, with short, blunted microvilli. These morphological criteria were used to diagnose WAS from the cord blood lymphocytes of one “at-risk” patient. Thus, WAS is the first primary immunodeficiency in which morphological abnormalities have been identified that can aid in diagnosis.