Journal articles on the topic 'B lymphocyte'
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1
Tait, Heidi. "Mechanisms behind the induction of Ttc7 transcription during B lymphocyte development(93.35)." Journal of Immunology 184, no. 1_Supplement (April 1, 2010): 93.35. http://dx.doi.org/10.4049/jimmunol.184.supp.93.35.
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Abstract Changes in Ttc7 (tetratricopeptide repeat domain 7) transcription have been associated with changes in B lymphocyte signaling through changes in both the lymphopoietic environment and homeostasis of B lymphocyte development in mice with the Ttc7fsn/fsn(flaky skin) mutation. We have demonstrated that young Ttc7fsn/fsn mice exhibit decreased naive B lymphocyte populations in the bone marrow and spleen as compared to their wild type littermates, and that this disparity is exaggerated with age. The Ttc7fsn/fsn mutation also leads to excessive production of harmful B1b lymphocytes causing autoimmune disease closely related to SLE. This is significant as both autoimmune and aging human populations share similar B lymphocyte profiles. The evaluation of signaling events upstream of Ttc7 transcription will shed light on stage-specific B cell developmental signaling mechanisms in the bone marrow and spleen that cause immunological dysfunction. We have begun to classify B lymphocyte stages at which Ttc7 transcription rates fluctuate in pursuit of these signaling mechanisms. We have found Ttc7 to be transcribed in the bone marrow at early B lymphocyte stages and have evidence that its transcription is repressed at later stages in the spleen. To further support the hypothesis that induction of Ttc7 transcription during B cell development occurs in early B lymphocytes, we have also found that a 1kb segment of the promoter induces a higher rate of transcription in the pre-B 70Z/3 cell line.
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M, Leclerc. "The Sea Star B Lymphocyte." Vaccines & Vaccination Open Access 8, no. 2 (August 4, 2023): 1–2. http://dx.doi.org/10.23880/vvoa-16000163.
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Milicevic, Novica. "T lymphocytes are necessary for the peripheral phase of B lymphocyte maturation." Srpski arhiv za celokupno lekarstvo 136, Suppl. 2 (2008): 166–70. http://dx.doi.org/10.2298/sarh08s2166m.
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Until recently, B lymphocyte maturation was considered to be independent of the thymus and T lymphocytes. However, using nude animals, which lack the functional thymus, we have shown that T lymphocytes are required for the peripheral phase of B lymphocyte maturation. We showed that the proportion of immature B lymphocyte subsets (CD90highIgMhigh and CD90highIgMlow) was significantly increased, whereas that of mature B lymphocyte subsets (CD90?IgMlow and CD90?IgMhigh) was decreased in the peripheral blood and lymph nodes of nude rats. In addition, the expression of functionally important surface molecules MHC class II, ICAM-1, CD44 and L-selectin was significantly down-regulated both on immature and mature B lymphocyte subsets. The implantation of thymic tissue under the kidney capsule of nude rats alleviated the block in B lymphocyte maturation and normalized of the defective expression of surface molecules. Comparable effects were seen after the adoptive transfer of T lymphocytes. This shows that in nude rats B lymphocytes do not mature properly due to the lack of T cell help and that T lymphocytes are required for the peripheral phase of B lymphocyte maturation, as well as for the appropriate expression of surface molecules. This should be considered when treating patients with T lymphocyte deficiencies.
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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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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, 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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HASEGAWA, Minoru. "B lymphocyte." Japanese Journal of Clinical Immunology 28, no. 5 (2005): 300–308. http://dx.doi.org/10.2177/jsci.28.300.
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Dorward, D. "Interactions Between Mouse Lymphocytes And Borrelia Burgdorferi, The Infectious Agent Of Lyme Disease." Microscopy and Microanalysis 5, S2 (August 1999): 1242–43. http://dx.doi.org/10.1017/s143192760001953x.
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Lyme disease is a tick borne, multi-system disorder caused by low density systemic infections with the spirochete Borrelia burgdorferi. Without antimicrobial treatment, mammalian infections with these bacteria are persistent and chronic. Recent studies showed that B. burgdorferi can target, invade, and lyse both cultured and primary human B and T cells. Direct interactions between the spirochetes and lymphocytes also leads to adherence of B and T cell antigens on the surface of significant proportions of the bacteria . Adherent lymphocytic antigens inhibit binding of antibodies to prominent B. burgdorferi proteins, and interfere with classic complement-mediated killing, suggesting a possible role for spirochete-lymphocyte interactions in immune evasion.In order to develop an experimental animal model for assessing spirochete-lymphocyte interactions, B. burgdorferi and primary mouse lymphocytes were co-incubated and examined by electron microscopy. Mononuclear cells were separated from fresh mouse blood by Ficoll gradient centrifugation (ICN, Biomedicals, Aurora, Ohio).
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Wang, Hui, Li Hong, Yangyang Tang, Meizhen Xu, Shuai Pan, Qingling Wang, and Cheng He. "Generation of a B-1 lymphocyte-specific conditional knockout mouse model Bhlhe41tdTomato-Cre." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 130.40. http://dx.doi.org/10.4049/jimmunol.202.supp.130.40.
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Abstract B-1 lymphocytes play indispensable roles in defensing a wide range of pathogens prior to adaptive immune response arising. Although several transgenic mouse models targeting different stages of B lymphocytes have been established e.g. Cd19-Cre and Mb1-Cre, a B-1 lymphocyte specific conditional knockout mouse model for illuminating the role of a gene of interest in B-1 lymphocytes is still missing. In this study, we aimed to generate a B-1 lymphocyte-specific knockout mouse model by expression of Cre recombinase under the control of the promoter of Bhlhe41, which is preferentially expressed in B-1 lymphocyte and microglia in immune system. A tdTomato-2A-Cre-polyA cassette was inserted to the locus of Bhlhe41 by CRISPR-CAS9 technology. Bhlhe41tdTomato-Cre/+Rosa26EYFP/+ mice were generated for determining Cre-mediated recombination efficiency. The accuracy of insertion of tdTomato-2A-Cre-polyA cassette to Bhlhe41 locus was confirmed by significantly reduced peritoneal B-1a lymphocytes in Bhlhe41tdTomato-Cre/tdTomato-Cre mice. Flow cytometric analysis of tdTomato in immune cells from Bhlhe41tdTomato-Cre/+confirmed the specific expression of BHLHE41 in B-1 lymphocytes rather than other B subsets. Further analysis of EYFP in immune cells from Bhlhe41tdTomato-Cre/+Rosa26EYFP/+ mice revealed larger than 90% recombination in splenic and peritoneal B-1 lymphocytes while less than 10% recombination in other B subsets. Hence, we generated a B-1 lymphocyte-specific conditional knockout mouse model Bhlhe41tdTomato-Cre, which can be used for studying the function of a specific gene in B-1 lymphocyte-mediated immune responses.
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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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Barrington, Robert A., Olga Pozdnyakova, Mohammad R. Zafari, Christopher D. Benjamin, and Michael C. Carroll. "B Lymphocyte Memory." Journal of Experimental Medicine 196, no. 9 (October 28, 2002): 1189–200. http://dx.doi.org/10.1084/jem.20021110.
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To dissect the influence of CD21/CD35 and FcγRIIB in antigen retention and humoral memory, we used an adoptive transfer model in which antigen-primed B and T lymphocytes were given to sublethally irradiated wild-type mice or mice deficient in CD21/CD35 (Cr2−/−) or FcγRIIB receptors (FcγRIIB−/−). Cr2−/− chimeras showed impaired memory as characterized by a decrease in antibody titer, reduced frequency of antibody secreting cells, an absence of affinity maturation, and significantly reduced recall response. The impaired memory in Cr2−/− chimeras corresponded with the reduced frequency of antigen-specific memory B cells. Interestingly, FcγRIIB−/− chimeras showed a differential phenotype with impaired splenic but normal bone marrow responses. These data suggest that CD21/CD35 on stroma, including follicular dendritic cells, is critical to the maintenance of long-term B lymphocyte memory.
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Roth, R., and M. J. Mamula. "Trafficking of adoptively transferred B lymphocytes in B-lymphocyte-deficient mice." Journal of Experimental Biology 200, no. 14 (July 1, 1997): 2057–62. http://dx.doi.org/10.1242/jeb.200.14.2057.
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Many studies have investigated the fate of adoptively transferred lymphocytes in recipient mice, although little is known of the sites where these transferred cells reside at particular time points. Using flow cytometry, we analyzed the trafficking pattern of adoptively transferred naive B cells into the lymphoid organs of syngeneic B-cell-deficient (microMT) mice. Within the first 24 h of transfer, the location of B cells was highly dependent on the mode of B-cell transfer. When B cells were injected subcutaneously into microMT mice, they showed a different trafficking pattern from cells administered into the peritoneal cavity or injected intravenously. After subcutaneous transfer into the thigh, the greatest number of B cells was detected in the popliteal lymph node nearest to the injection site, whereas the lowest number was detected in the axillary lymph node opposite to the injection side. Within the first 24 h of either intraperitoneal and intravenous injection, B cells were found in approximately equal numbers in the lymph nodes and the spleen. Two days later, the B-cell distribution in the lymphoid organs appeared to be independent of the mode of B-cell transfer. A transient decrease in the numbers of splenic and lymph node B cells occurred 9 days after B-cell transfer (a decrease from 70 to 87%) prior to the outgrowth of B cells that occurs 21 days after transfer. These studies are useful for understanding the numbers of B cells that may be required in adoptive transfer studies and their potential cellular interactions at particular physiological sites based on the route of cell transfer.
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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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Yang, Jiale, Xiaojian Zhu, and Jun Feng. "The Changes in the Quantity of Lymphocyte Subpopulations during the Process of Sepsis." International Journal of Molecular Sciences 25, no. 3 (February 5, 2024): 1902. http://dx.doi.org/10.3390/ijms25031902.
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Sepsis remains a global challenge, especially in low- and middle-income countries, where there is an urgent need for easily accessible and cost-effective biomarkers to predict the occurrence and prognosis of sepsis. Lymphocyte counts are easy to measure clinically, and a large body of animal and clinical research has shown that lymphocyte counts are closely related to the incidence and prognosis of sepsis. This review extensively collected experimental articles related to lymphocyte counts since the unification of the definition of sepsis. The article categorizes and discusses the relationship between absolute lymphocyte counts, intrinsic lymphocyte subsets, effector T-lymphocytes, B-lymphocytes, dendritic cells, and the incidence and prognosis of sepsis. The results indicate that comparisons of absolute lymphocyte counts alone are meaningless. However, in addition to absolute lymphocyte counts, innate lymphocyte subsets, effector T-cells, B-lymphocytes, and dendritic cells have shown certain research value in related studies.
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Denis, K. A., K. Dorshkind, and O. N. Witte. "Regulated progression of B lymphocyte differentiation from cultured fetal liver." Journal of Experimental Medicine 166, no. 2 (August 1, 1987): 391–403. http://dx.doi.org/10.1084/jem.166.2.391.
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Lymphoid fetal liver cultures (LFLC) are long-term, nontransformed cultures of early B lymphoid lineage cells which appear developmentally blocked at the pre-B stage in vitro. When injected into severe combined immunodeficient (SCID) mice, cells from LFLC could reconstitute splenic B lymphocytes and serum IgM. T lymphocyte reconstitution was not observed and serum IgG levels were very low. IgG3 was the predominant gamma subisotype in the serum of the LFLC-reconstituted mice, indicating impaired class switching in these B lymphocytes. When thymocytes were coinjected with LFLC, the B lymphocytes were able to class switch fully and respond to T-dependent antigens. These serological responses were heterogeneous. This experimental system allows separation of three B lymphocyte developmental stages: early differentiation in vitro, progression to IgM secretion in vivo, and late differentiation dependent upon mature T lymphocytes in vivo. The unique advantage of this system is the ability to regulate the B lymphocyte developmental pathway in a defined, stepwise manner.
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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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Ishihara, Katsuhiko, Kay Medina, Shin-Ichi Hayashi, Carolynn Pietrangeli, Anthony E. Namen, Kensuke Miyake, and Paul W. Kincade. "Stromal-Cell and Cytokine-Dependent Lymphocyte Clones Which Span the Pre-B- to B-Cell Transition." Developmental Immunology 1, no. 3 (1991): 149–61. http://dx.doi.org/10.1155/1991/79721.
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Five stromal-cell-dependent lymphocyte clones are described that correspond to late pre-B or early B-cell stages of differentiation.They are useful for determining the molecular requirements for pre-B replication, for studying the stromal cells that supply those factors, and for delineating the final sequence of differentiation events as newly formed lymphocytes prepare to exit the bone marrow. The efficiency of lymphocyte growth at limiting dilution varied substantially on different stromal-cell clones and may reflect functional heterogeneity of stromal cells. Most lymphocyte clones were similar to uncloned lymphocytes from Whitlock-Witte cultures in that they responded only transiently to interleukin-7 (IL-7) and then died, unless maintained on a stromal-cell clone. One unusual lymphocyte clone (2E8) was propagated for more than 1 year in IL-7 alone and was selectively responsive to that cytokine. Most of the lymphocyte clones were not tumorigenic in immunodeficient mice. However, one pre-B clone (1A9)’grew autonomously in culture when held at high density, responded to conditioned medium from a number of cell lines, and was tumorigenic. Tumors derived from this clone were infiltrated by stromal cells and lymphocytes taken from the tumors' retained characteristics of the original clone. Ly-6 antigens were inducible on 2E8 and 1A9 cells, but the lymphocytes were otherwise arrested in differentiation. The 2E8 cells had rearranged and expressedκlight-chain genes but displayed them on the surface along with surrogate light chains andμheavy chains. Thus, expression of authentic Tight chain need not coincide with termination of surrogate light-chain utilization in newly formed B cells. Several glycoproteins have recently been demonstrated to be associated with surface immunoglobulin (Ig) on mature B-lineage cells and plasma-cell tumors. We now show that one member of this family (approximately 33 kD) was associated with theμ+surrogate light-chain complex on the 1A9 pre-B-cell clone. When compared to mature B lymphomas, fewer bands coprecipitated with the surface-labeled Ig isolated from pre-B- and early B-cell lines, suggesting that components of the antigen receptor are sequentially acquired during development. The normal replication and differentiation of pre-B cells is probably regulated by complex interactions with multiple cytokines and matrix components of the marrow microenvironment. Cloned lymphocyte lines that are dependent on stromal cells should continue to be important tools for molecular definition of those interactions.
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Kurosaki, Tomohiro. "B-lymphocyte biology." Immunological Reviews 237, no. 1 (August 19, 2010): 5–9. http://dx.doi.org/10.1111/j.1600-065x.2010.00946.x.
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Nel, A. E., M. W. Wooten, G. E. Landreth, P. J. Goldschmidt-Clermont, H. C. Stevenson, P. J. Miller, and R. M. Galbraith. "Translocation of phospholipid/Ca2+-dependent protein kinase in B-lymphocytes activated by phorbol ester or cross-linking of membrane immunoglobulin." Biochemical Journal 233, no. 1 (January 1, 1986): 145–49. http://dx.doi.org/10.1042/bj2330145.
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Stimulation of peripheral-blood B-lymphocytes with phorbol ester or anti-immunoglobulin demonstrated intracellular translocation of phospholipid/Ca2+-dependent protein kinase (C-kinase) activity from cytosol to membrane fractions. This phenomenon, which was dose- and time-dependent, was found in both normal and chronic-lymphocytic-leukemia B-cells. This suggests that C-kinase-dependent protein phosphorylation may be related to membrane receptor occupation and may therefore be important in B-lymphocyte responses.
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Reid, G. K., and D. G. Osmond. "B lymphocyte production in the bone marrow of mice with X-linked immunodeficiency (xid)." Journal of Immunology 135, no. 4 (October 1, 1985): 2299–302. http://dx.doi.org/10.4049/jimmunol.135.4.2299.
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Abstract CBA/N mice carry an X-linked recessive immunodeficiency (xid) gene manifested by the absence of a B lymphocyte subpopulation, but the manner in which the xid gene exerts its effect on B lymphocyte development is unknown. The production of B lymphocytes in the bone marrow of CBA/N mice has now been compared with that of normal CBA/J mice by using two in vivo assays: immunofluorescence stathmokinetic studies measured pre-B cell proliferation, whereas radioautographic [3H]thymidine labeling was used to evaluate small lymphocyte turnover. Although the total cellularity of CBA/N mouse bone marrow was greater than normal, the absolute number of marrow small lymphocytes, pre-B cells, and B lymphocytes were all similar to those in CBA/J controls. Furthermore, in the bone marrow of CBA/N mice, the proliferation rate of pre-B cells, calculated from their rate of entry into mitosis, and the turnover rate of small lymphocytes, derived from their rate of [3H]thymidine labeling, were not significantly different from those seen in nondefective mice. The present findings that pre-B cell proliferation and small lymphocyte production proceed at similar rates in the bone marrow of xid and normal mice suggest that the xid gene does not act at the level of primary B cell genesis in the bone marrow. The findings are in accord with the view that the xid gene produces a maturation block or a functional abnormality among B lymphocytes in the peripheral lymphoid tissues rather than the deletion of a sublineage of B lymphocytes in the bone marrow.
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Janker, Stefanie, Simon Doswald, Roman R. Schimmer, Urs Schanz, Wendelin J. Stark, Martin Schläpfer, and Beatrice Beck-Schimmer. "Targeted Large-Volume Lymphocyte Removal Using Magnetic Nanoparticles in Blood Samples of Patients with Chronic Lymphocytic Leukemia: A Proof-of-Concept Study." International Journal of Molecular Sciences 24, no. 8 (April 19, 2023): 7523. http://dx.doi.org/10.3390/ijms24087523.
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In the past, our research group was able to successfully remove circulating tumor cells with magnetic nanoparticles. While these cancer cells are typically present in low numbers, we hypothesized that magnetic nanoparticles, besides catching single cells, are also capable of eliminating a large number of tumor cells from the blood ex vivo. This approach was tested in a small pilot study in blood samples of patients suffering from chronic lymphocytic leukemia (CLL), a mature B-cell neoplasm. Cluster of differentiation (CD) 52 is a ubiquitously expressed surface antigen on mature lymphocytes. Alemtuzumab (MabCampath®) is a humanized, IgG1κ, monoclonal antibody directed against CD52, which was formerly clinically approved for treating chronic lymphocytic leukemia (CLL) and therefore regarded as an ideal candidate for further tests to develop new treatment options. Alemtuzumab was bound onto carbon-coated cobalt nanoparticles. The particles were added to blood samples of CLL patients and finally removed, ideally with bound B lymphocytes, using a magnetic column. Flow cytometry quantified lymphocyte counts before, after the first, and after the second flow across the column. A mixed effects analysis was performed to evaluate removal efficiency. p < 0.05 was defined as significant. In the first patient cohort (n = 10), using a fixed nanoparticle concentration, CD19-positive B lymphocytes were reduced by 38% and by 53% after the first and the second purification steps (p = 0.002 and p = 0.005), respectively. In a second patient cohort (n = 11), the nanoparticle concentration was increased, and CD19-positive B lymphocytes were reduced by 44% (p < 0.001) with no further removal after the second purification step. In patients with a high lymphocyte count (>20 G/L), an improved efficiency of approximately 20% was observed using higher nanoparticle concentrations. A 40 to 50% reduction of B lymphocyte count using alemtuzumab-coupled carbon-coated cobalt nanoparticles is feasible, also in patients with a high lymphocyte count. A second purification step did not further increase removal. This proof-of-concept study demonstrates that such particles allow for the targeted extraction of larger amounts of cellular blood components and might offer new treatment options in the far future.
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Mun, Yeung-Chul, Kyoung-Eun Lee, Jung Mi Kwon, Seung-Hyun Nam, Eun Sun Yoo, Yun-Kyung Bae, Seung-Eun Lee, et al. "Establishment of Effective B Lymphocyte Ex Vivo Expansion on Human Cord Blood Using TPO, SCF, FL, IL-4, IL-10, and CD40L." Blood 104, no. 11 (November 16, 2004): 2882. http://dx.doi.org/10.1182/blood.v104.11.2882.2882.
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Abstract In respect to B lymphocyte-mediated immunity, characteristics of human cord blood are low counts of mature B lymphocytes, deficient expression of CD40L and cytokine production in CD4+ T lymphocytes, defect in the isotype switch of immunoglobulin and the activation of B lymphocytes, and low IgG production of B lymphocytes. These characteristics of the B lymphocyte from human cord blood lead to a delayed B lymphocyte-mediated immune reconstitution and an increased susceptibility to infections after a cord blood transplantation. The mechanism of immunological recostitution after cord blood transplantation has been examined from a variety of viewpoints in experimental models as well as clinical studies. However, problems of sustained immunodeficiency after cord blood transplantation remain to be resolved. The aim of the present study is to establish culture conditions that support the effective B lymphocyte expansion of human cord blood using IL-4, IL-10, and CD40L, to which cytokines are defected in B lymphocyte of human cord blood, and established conditions are compared to previously established cytokine combinations, TPO+SCF+FL in our Lab (Br J Haematol 107:176–185, 1999 & Stem Cells 21:228–235, 2003). To elucidate the effective B lymphocyte-mediated immune reconstitution of cord blood after ex vivo expansion, mononuclear cells, separated from density gradient of Ficoll system, and CD34+ purified cells, isolated from immunomicrobead(MiniMACS) system, were cultured with various combinations of cytokines (TPO+FL+SCF and/or IL-4, IL-10 and CD40L) for 2 weeks or 4 weeks. This then allowed for cytometric analysis after immunofluorescence stain with CD34, CD38 (for HSC analysis) and CD19, IgG and IgM (for B lymphocyte-mediated immune reconstitution) and CD4 (for T helper cell) and CD25 (for lymphocyte activation assay) to be performed. In the B lymphocyte expansion aspect, the immunoglobulin expression, and functional activity, expansion with the TPO+FL+SCF+IL-4+IL-10 combination showed best results in the expression of CD19, CD25, IgG, and IgM. However, the addition of CD40L to those culture condition did not increase expression of CD19, CD25, IgG, and IgM after the expansion of human cord blood. Expansion of CD34+ purified cells was superior to MNCs in the expression of CD19, CD25, IgG, and IgM. In consideration for the duration of cultures, the 2 week culture was superior to the 4 week culture with respect to graft stemness (CD34+CD38- fraction). Our data suggests most superior results were observed from the ex vivo expansion of CD34+ purified cells cultured for 2 weeks with TPO+FL+SCF+IL-4+IL-10, in the B lymphocyte-mediated immune reconstitution and graft stemness aspect. The results of this study warrant further investigation on effective B lymphocyte-mediated immune reconstitution after cord blood transplantation in vivo using ex vivo expanded cord blood.
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van Zelm, Menno C., Tomasz Szczepański, Mirjam van der Burg, and Jacques J. M. van Dongen. "Replication history of B lymphocytes reveals homeostatic proliferation and extensive antigen-induced B cell expansion." Journal of Experimental Medicine 204, no. 3 (February 20, 2007): 645–55. http://dx.doi.org/10.1084/jem.20060964.
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The contribution of proliferation to B lymphocyte homeostasis and antigen responses is largely unknown. We quantified the replication history of mouse and human B lymphocyte subsets by calculating the ratio between genomic coding joints and signal joints on kappa-deleting recombination excision circles (KREC) of the IGK-deleting rearrangement. This approach was validated with in vitro proliferation studies. We demonstrate that naive mature B lymphocytes, but not transitional B lymphocytes, undergo in vivo homeostatic proliferation in the absence of somatic mutations in the periphery. T cell–dependent B cell proliferation was substantially higher and showed higher frequencies of somatic hypermutation than T cell–independent responses, fitting with the robustness and high affinity of T cell–dependent antibody responses. More extensive proliferation and somatic hypermutation in antigen-experienced B lymphocytes from human adults compared to children indicated consecutive responses upon additional antigen exposures. Our combined observations unravel the contribution of proliferation to both B lymphocyte homeostasis and antigen-induced B cell expansion. We propose an important role for both processes in humoral immunity. These new insights will support the understanding of peripheral B cell regeneration after hematopoietic stem cell transplantation or B cell–directed antibody therapy, and the identification of defects in homeostatic or antigen-induced B cell proliferation in patients with common variable immunodeficiency or another antibody deficiency.
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Kaur, Amitinder, Michele Di Mascio, Amy Barabasz, Michael Rosenzweig, Harold M. McClure, Alan S. Perelson, Ruy M. Ribeiro, and R. Paul Johnson. "Dynamics of T- and B-Lymphocyte Turnover in a Natural Host of Simian Immunodeficiency Virus." Journal of Virology 82, no. 3 (November 21, 2007): 1084–93. http://dx.doi.org/10.1128/jvi.02197-07.
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ABSTRACT Increased lymphocyte turnover is a hallmark of pathogenic lentiviral infection. To investigate perturbations in lymphocyte dynamics in natural hosts with nonpathogenic simian immunodeficiency virus (SIV) infection, the nucleoside analog bromodeoxyuridine (BrdU) was administered to six naturally SIV-infected and five SIV-negative sooty mangabeys. As a measure of lymphocyte turnover, we estimated the mean death rate by fitting a mathematical model to the fraction of BrdU-labeled cells during a 2-week labeling and a median 10-week delabeling period. Despite significantly lower total T- and B-lymphocyte counts in SIV-infected sooty mangabeys than in SIV-negative mangabeys, the turnover rate of B lymphocytes and CD4+ and CD8+ T lymphocytes was not increased in the SIV-infected animals. A small, rapidly proliferating CD45RA+ memory subset and a large, slower-proliferating CD45RA− central memory subset of CD4+ T lymphocytes identified in the peripheral blood of sooty mangabeys also did not show evidence of increased turnover in the context of SIV infection. Independently of SIV infection, the turnover of CD4+ T lymphocytes in sooty mangabeys was significantly higher (P < 0.01) than that of CD8+ T lymphocytes, a finding hitherto not reported in rhesus macaques or humans. The absence of aberrant T-lymphocyte turnover along with an inherently high rate of CD4+ T-lymphocyte turnover may help to preserve the pool of central memory CD4+ T lymphocytes in viremic SIV-infected sooty mangabeys and protect against progression to AIDS.
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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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Uher, F., and H. B. Dickler. "Interactions between B lymphocyte subpopulations. Augmentation of the responses of resting B lymphocytes by activated B lymphocytes." Journal of Immunology 140, no. 5 (March 1, 1988): 1442–47. http://dx.doi.org/10.4049/jimmunol.140.5.1442.
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Abstract Mouse B lymphocytes were fractionated from normal T lymphocyte-depleted spleen cell populations using discontinuous percoll gradients and were stimulated with rabbit F(ab')2 anti-mouse mu-specific antibodies (anti-mu) plus the supernatant of Con A-stimulated rat spleen cells (SN) as a source of lymphokines. The responses of small (mean volume 120 mu 3), dense (greater than 1.087 specific gravity), resting (least spontaneous thymidine incorporation) B lymphocytes were augmented by irradiated (4000 rad), larger (mean volume greater than 170 mu 3), less dense (less than 1.081 specific gravity), activated (greater spontaneous thymidine incorporation) B lymphocytes. Proliferation was augmented 2- to 4-fold and polyclonal antibody-forming cell responses three- to sixfold. Maximal augmentation of the responses of 5 X 10(4) resting B cells was obtained with 10(4) activated B cells. Augmenting activity was specific for activated B lymphocytes in that responses were not augmented by irradiated thymocytes, T lymphoblasts, macrophages, or additional supernatant. B lymphocytes activated in vitro by LPS or anti-mu also had augmenting activity. Augmentation of responses was maximal only when activated B lymphocytes were added simultaneously with anti-mu. The interaction between activated and resting B lymphocytes did not appear to be genetically restricted. Interestingly, the augmenting activity of activated B cells could be reconstituted by a combination of supernatant and cell membranes from these cells but not by either alone, suggesting that two components are required, one soluble and the other membrane-bound. Thus, a functional interaction has been demonstrated between B lymphocyte subpopulations which differ in their state of activation, and this interaction appears to involve a novel mechanism of action.
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Karabon, L., A. Partyka, L. Ciszak, E. Pawlak-Adamska, A. Tomkiewicz, A. Bojarska-Junak, J. Roliński, et al. "Abnormal Expression of BTLA and CTLA-4 Immune Checkpoint Molecules in Chronic Lymphocytic Leukemia Patients." Journal of Immunology Research 2020 (July 28, 2020): 1–12. http://dx.doi.org/10.1155/2020/6545921.
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Chronic lymphocytic leukemia (CLL) is characterized by the peripheral accumulation of neoplastic B cells and is frequently complicated by the systemic immunosuppression associated with an impairment in B and T lymphocyte activation. We hypothesized that the expression of immune checkpoint suppressors B and T lymphocyte attenuator (BTLA) and cytotoxic T lymphocyte antigen (CTLA-4) is disturbed in both lymphocyte subpopulations in CLL. The expression of CTLA-4 and BTLA mRNA was determined by real-time PCR, while CTLA-4 protein expression (surface or intracellular) was estimated in BTLA+ lymphocytes by flow cytometry. In CLL patients, we observed a higher gene transcript level of BTLA and CTLA-4 than in healthy individuals in both freshly isolated and PMA stimulated B and T cells. Remarkably, lower amounts of both inhibitory proteins were found in peripheral blood (PB) CLL B cells, whereas normal BTLA and elevated CTLA-4 were found in T cells. Consistently, there was a prevalence of CTLA-4+ cells within circulating BTLA+ T cells cells of patients confronting PB healthy cells. After in vitro stimulation, the only change found in CLL patients was a decrease in BTLA expression in B and T lymphocytes. In contrast, healthy lymphocytes responded more vigorously as regards the BTLA and CTLA expression with substantially higher frequency of CD69+ cells under the stimulating condition compared to corresponding cells from the CLL group. Our results indicate that CLL development is associated with the affected expression of BTLA and CTLA-4 checkpoint receptors in PB and its impaired expression might be associated with lowering of the threshold for B cell activation and proliferation, while upregulated CTLA-4 expression in CLL peripheral BTLA+ T cells may contribute to suppressed T cell effector functions. This hypothesis needs to be validated in future studies, which would allow us to explain how the increased or decreased expression of these molecules affects the cell function.
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Diniz, Vinicius Leonardo Sousa, Anuska Marcelino Alvares-Saraiva, Tamires Duarte Afonso Serdan, Laiane Cristina dos Santos-Oliveira, Vinicius Cruzat, Tiago Bertola Lobato, Richelieau Manoel, et al. "Essential metabolism required for T and B lymphocyte functions: an update." Clinical Science 137, no. 10 (May 2023): 807–21. http://dx.doi.org/10.1042/cs20220869.
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Abstract Lymphocytes act as regulatory and effector cells in inflammation and infection situations. A metabolic switch towards glycolytic metabolism predominance occurs during T lymphocyte differentiation to inflammatory phenotypes (Th1 and Th17 cells). Maturation of T regulatory cells, however, may require activation of oxidative pathways. Metabolic transitions also occur in different maturation stages and activation of B lymphocytes. Under activation, B lymphocytes undergo cell growth and proliferation, associated with increased macromolecule synthesis. The B lymphocyte response to an antigen challenge requires an increased adenosine triphosphate (ATP) supply derived mainly through glycolytic metabolism. After stimulation, B lymphocytes increase glucose uptake, but they do not accumulate glycolytic intermediates, probably due to an increase in various metabolic pathway ‘end product’ formation. Activated B lymphocytes are associated with increased utilization of pyrimidines and purines for RNA synthesis and fatty acid oxidation. The generation of plasmablasts and plasma cells from B lymphocytes is crucial for antibody production. Antibody production and secretion require increased glucose consumption since 90% of consumed glucose is needed for antibody glycosylation. This review describes critical aspects of lymphocyte metabolism and functional interplay during activation. We discuss the primary fuels for the metabolism of lymphocytes and the particularities of T and B cell metabolism, including the differentiation of lymphocytes, stages of development of B cells, and the production of antibodies.
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Clark, P., DE Normansell, DJ Innes, and CE Hess. "Lymphocyte subsets in normal bone marrow." Blood 67, no. 6 (June 1, 1986): 1600–1606. http://dx.doi.org/10.1182/blood.v67.6.1600.1600.
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Abstract Bone marrow aspirates and biopsies from ten normal donors were stained directly with monoclonal antibodies specific for lymphocyte, monocyte, and myeloid antigens, and were analyzed by flow cytometry. To avoid cell loss, lymphocytes were not specifically isolated prior to staining. T cells comprised 46% of aspirate lymphocytes and 22% of biopsy lymphocytes. Further, the Leu-3:Leu-2 ratio of bone marrow T cells was below 1.0. B cells comprised 8% to 11% of bone marrow lymphocytes in both aspirates and biopsies, and there was a substantial percentage of cells in the lymphocyte window that was negative for all B and T cell markers. The lymphocyte window had very little myeloid contamination; however, when the myeloid window was examined, staining was greater than 90%.
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Clark, P., DE Normansell, DJ Innes, and CE Hess. "Lymphocyte subsets in normal bone marrow." Blood 67, no. 6 (June 1, 1986): 1600–1606. http://dx.doi.org/10.1182/blood.v67.6.1600.bloodjournal6761600.
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Bone marrow aspirates and biopsies from ten normal donors were stained directly with monoclonal antibodies specific for lymphocyte, monocyte, and myeloid antigens, and were analyzed by flow cytometry. To avoid cell loss, lymphocytes were not specifically isolated prior to staining. T cells comprised 46% of aspirate lymphocytes and 22% of biopsy lymphocytes. Further, the Leu-3:Leu-2 ratio of bone marrow T cells was below 1.0. B cells comprised 8% to 11% of bone marrow lymphocytes in both aspirates and biopsies, and there was a substantial percentage of cells in the lymphocyte window that was negative for all B and T cell markers. The lymphocyte window had very little myeloid contamination; however, when the myeloid window was examined, staining was greater than 90%.
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Dang, L. H., and K. L. Rock. "Stimulation of B lymphocytes through surface Ig receptors induces LFA-1 and ICAM-1-dependent adhesion." Journal of Immunology 146, no. 10 (May 15, 1991): 3273–79. http://dx.doi.org/10.4049/jimmunol.146.10.3273.
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Abstract Engagement of the surface Ig receptor with anti-IgM antibodies stimulates murine B lymphocytes to markedly increase their expression of the cell adhesion molecules ICAM-1 and LFA-1. Stimulated B cells display increased homotypic adhesiveness and form spontaneous heterotypic conjugates with T lymphocytes. This latter T-B cell interaction is further enhanced if T cells have been previously activated with phorbol esters. In all cases, the formation of cell-cell conjugates is dependent on LFA-1-ICAM-1-mediated interactions as assessed in mAb blocking experiments. B lymphocytes stimulated with anti-IgM display a marked increase in binding to ICAM-1-transfected L cells. This cell-cell interaction is inhibited by anti-LFA-1 mAb binding to the B lymphocyte. Together, these results demonstrate that there is an induction of both ICAM-1 and LFA-1 on stimulated B cells and a corresponding increase in the adhesiveness of these cells. These findings suggest that Ag binding to the surface Ig receptor could prepare a B lymphocyte for subsequent interaction with a T lymphocyte. This provides insight into how efficient T-B collaboration may occur between very infrequent Ag-specific lymphocytes.
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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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Carvalho, Thiago L., Tomaz Mota-Santos, Ana Cumano, Jocelyne Demengeot, and Paulo Vieira. "Arrested B Lymphopoiesis and Persistence of Activated B Cells in Adult Interleukin 7−/− Mice." Journal of Experimental Medicine 194, no. 8 (October 15, 2001): 1141–50. http://dx.doi.org/10.1084/jem.194.8.1141.
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Interleukin 7 is a crucial factor for the development of murine T and B lymphocytes. We now report that, in the absence of interleukin 7, B lymphocyte production takes place exclusively during fetal and perinatal life, ceasing after 7 wk of age. In peripheral organs, however, the pool of B lymphocytes is stable throughout adult life and consists only of cells that belong to the B1 and marginal zone (MZ) compartments. This is accompanied by a 50-fold increase in the frequency of immunoglobulin (Ig)M- and IgG-secreting cells, and the concentration of serum immunoglobulins is increased three- to fivefold. Both the MZ phenotype and the increase in serum IgM are T cell independent. These findings reveal a previously undescribed pathway of B lymphopoiesis that is active in early life and is interleukin 7 independent. This pathway generates B1 cells and a normal sized MZ B lymphocyte compartment.
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Kusunoki, Y., Y. Kodama, Y. Hirai, S. Kyoizumi, N. Nakamura, and M. Akiyama. "Cytogenetic and immunologic identification of clonal expansion of stem cells into T and B lymphocytes in one Atomic-bomb survivor." Blood 86, no. 6 (September 15, 1995): 2106–12. http://dx.doi.org/10.1182/blood.v86.6.2106.bloodjournal8662106.
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Chromosome aberration frequency in peripheral blood lymphocytes is elevated in radiation-exposed people, and identical karyotypic changes are not infrequently encountered in one blood sample as well as in separate samples from the same donor. Such clonal propagation originates either from a single immature stem cell able to expand and differentiate into several cell types or from a single mature lymphocyte able to expand after antigen stimulation in vivo. In the present study, a total 71 T-lymphocyte and 58 B-lymphocyte colonies were established from one atomic-bomb survivor, who showed a persistent clonal aberration t(4;6), t(5;13) in phytohemagglutinin culture of peripheral lymphocytes. Nearly 10% of the colonies (6 T-lymphocyte and 7 B-lymphocyte colonies) showed the same chromosome abnormality. Southern blot analyses of the T-cell-receptor or Ig heavy-chain gene showed all different rearrangement patterns among T- or B-lymphocyte colonies, respectively. Thus, the chromosome aberration occurred in a precursor cell before differentiation into T and B lineages and was not derived from monoclonal proliferation of mature T or B lymphocytes in the periphery. To confirm the issue, cells from erythroid burst-forming unit (BFU-E) colonies were examined by the chromosome-painting method. Two translocations, one between chromosomes 5 and 13 and the other between chromosomes 4 and one of group C, perfectly consistent with the t(4;6), t(5;13), were found in about 10% of the cells. The results imply that a single stem cell of an adult is capable of generating long- lived myeloid and lymphoid progeny amounting to several percent of the total population of circulating lymphocytes and hematopoietic progenitors.
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Klein da Costa, Bruna, Renata Brant de Souza Melo, Giordani Rodrigues dos Passos, Douglas Gomes Meneses Sevilha Castro, Jefferson Becker, Amit Bar-Or, and Douglas Kazutoshi Sato. "Unraveling B lymphocytes in CNS inflammatory diseases." Neurology 95, no. 16 (September 9, 2020): 733–44. http://dx.doi.org/10.1212/wnl.0000000000010789.
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Specific therapies targeting B lymphocytes in multiple sclerosis (MS) have demonstrated reductions in disease activity and disability progression. Several observational studies have also shown the effects of targeting B lymphocytes in other rare CNS inflammatory diseases, such as neuromyelitis optica spectrum disorder (NMOSD) and autoimmune encephalitis (AE). However, some drugs targeting cytokine receptors involved in B-lymphocyte maturation and proliferation resulted in negative outcomes in MS. These apparently conflicting findings have stimulated research on the pathophysiologic mechanisms of B lymphocytes in CNS inflammatory diseases. It has been demonstrated that B lymphocytes participate in the pathogenesis of these conditions as antigen-presenting cells, producing proinflammatory cytokines that induce Th1 and Th17 responses and producing antibodies. However, they are also able to produce anti-inflammatory cytokines, such as interleukin-10, functioning as regulators of autoimmunity. Understanding these diverse effects is essential for the development of focused treatments. In this review, we discuss the possible mechanisms that underlie B-lymphocyte involvement in MS, NMOSD, and AE and the outcomes obtained by treatments targeting B lymphocytes.
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Trueblood, Esther S., Wendy C. Brown, Guy H. Palmer, William C. Davis, Diana M. Stone, and Terry F. McElwain. "B-Lymphocyte Proliferation during Bovine Leukemia VirusInduced Persistent Lymphocytosis Is Enhanced by T-Lymphocyte-Derived Interleukin-2." Journal of Virology 72, no. 4 (April 1, 1998): 3169–77. http://dx.doi.org/10.1128/jvi.72.4.3169-3177.1998.
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ABSTRACT Bovine leukemia virus (BLV)-induced persistent lymphocytosis is characterized by a polyclonal expansion of CD5+ B lymphocytes. To examine the role of the cytokine microenvironment in this virus-induced B-lymphocyte expansion, the expression of interleukin-2 (IL-2), IL-4, IL-10, and gamma interferon (IFN-γ) mRNA, was measured in stimulated peripheral blood mononuclear cells from persistently lymphocytotic BLV-infected cows, nonlymphocytotic BLV-infected cows, and uninfected cows. IL-2 and IL-10 mRNA expression and IL-2 functional activity were significantly increased when peripheral blood mononuclear cells from persistently lymphocytotic cows were stimulated with concanavalin A (ConA). Additionally, during persistent lymphocytosis, peak IL-2 and IL-10 mRNA expression was delayed, and elevated expression was prolonged. To determine the potential biologic importance of increased IL-2 and IL-10 expression, the response of isolated B lymphocytes from persistently lymphocytotic cows to human recombinant cytokines and to cytokine-containing supernatants from isolated T lymphocytes was examined. While recombinant human IL-10 (rhIL-10) did not consistently induce detectable changes, rhIL-2 increased viral protein (p24) and IL-2 receptor expression in isolated B lymphocytes from persistently lymphocytotic cows. Additionally, rhIL-2 and supernatant from ConA-stimulated T lymphocytes enhanced B-lymphocyte proliferation. The stimulatory activity of the T-lymphocyte supernatant could be completely inhibited with a polyclonal anti-rhIL-2 antibody. Finally, polyclonal anti-rhIL-2 antibody, as well as anti-BLV antibody, inhibited spontaneous proliferation of peripheral blood mononuclear cells from persistently lymphocytotic cows, demonstrating that the spontaneous lymphoproliferation characteristic of BLV-induced persistent lymphocytosis is IL-2 dependent and antigen dependent. Collectively, these findings strongly suggest that increased T-lymphocyte expression of IL-2 in BLV-infected cows contributes to development and/or maintenance of persistent B lymphocytosis.
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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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Hammerschmidt, DE, C. Jeanneret, M. Husak, M. Lobell, and HS Jacob. "Lymphocyte aggregation in response to adrenergic stimulation." Blood 71, no. 5 (May 1, 1988): 1470–74. http://dx.doi.org/10.1182/blood.v71.5.1470.1470.
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Abstract A nonanemic chronic lymphocytic leukemia patient with nearly 500,000 lymphocytes/microL underwent leukapheresis when she presented with CNS symptoms and retinal vascular engorgement. Respiratory distress developed during the cell separator run, which led us to ask whether the procedure could have changed the adhesive properties of her cells. C5a desarginine, N-f-Met-Leu-Phe, adenosine diphosphate, and collagen all failed to aggregate her lymphocytes in vitro, but arachidonic acid, excess free calcium, and 4 mumol/L epinephrine did aggregate the cells. Arachidonate-induced aggregation appeared to be a toxic phenomenon: the ED50 for aggregation was statistically indistinguishable from that for cytotoxicity, and aspirin only mildly blunted the response. In contrast, epinephrine-induced aggregation was not associated with lactic dehydrogenase release or the loss of trypan blue exclusion and was blunted by propranolol; radiopindolol-binding studies confirmed the presence of a beta-adrenergic receptor. There were approximately 3,000 receptors/cell, with no statistically significant difference between normal and chronic lymphocytic leukemia B cells or between B cells and T cells (separated by rosetting techniques). The Kd for the B cells' receptor, however, was less than that for T cells by a factor of ten (P less than .01). We conclude that B cells may aggregate when stimulated and that they--like T cells--have beta-adrenergic receptors. Adrenergically mediated changes in B cell adhesiveness may play a role in regulating lymphocyte traffic; in the rare patient with truly enormous B cell counts, we postulate that they may be an occasional cause of morbidity.
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Hammerschmidt, DE, C. Jeanneret, M. Husak, M. Lobell, and HS Jacob. "Lymphocyte aggregation in response to adrenergic stimulation." Blood 71, no. 5 (May 1, 1988): 1470–74. http://dx.doi.org/10.1182/blood.v71.5.1470.bloodjournal7151470.
Full textAbstract:
A nonanemic chronic lymphocytic leukemia patient with nearly 500,000 lymphocytes/microL underwent leukapheresis when she presented with CNS symptoms and retinal vascular engorgement. Respiratory distress developed during the cell separator run, which led us to ask whether the procedure could have changed the adhesive properties of her cells. C5a desarginine, N-f-Met-Leu-Phe, adenosine diphosphate, and collagen all failed to aggregate her lymphocytes in vitro, but arachidonic acid, excess free calcium, and 4 mumol/L epinephrine did aggregate the cells. Arachidonate-induced aggregation appeared to be a toxic phenomenon: the ED50 for aggregation was statistically indistinguishable from that for cytotoxicity, and aspirin only mildly blunted the response. In contrast, epinephrine-induced aggregation was not associated with lactic dehydrogenase release or the loss of trypan blue exclusion and was blunted by propranolol; radiopindolol-binding studies confirmed the presence of a beta-adrenergic receptor. There were approximately 3,000 receptors/cell, with no statistically significant difference between normal and chronic lymphocytic leukemia B cells or between B cells and T cells (separated by rosetting techniques). The Kd for the B cells' receptor, however, was less than that for T cells by a factor of ten (P less than .01). We conclude that B cells may aggregate when stimulated and that they--like T cells--have beta-adrenergic receptors. Adrenergically mediated changes in B cell adhesiveness may play a role in regulating lymphocyte traffic; in the rare patient with truly enormous B cell counts, we postulate that they may be an occasional cause of morbidity.
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Nasisse, Mark P., Robert V. English, Mary B. Tompkins, James S. Guy, and Wendy Sussman. "Immunologic, histologic, and virologic features of herpesvirus-induced stromal keratitis in cats." American Journal of Veterinary Research 56, no. 1 (January 1, 1995): 51–55. http://dx.doi.org/10.2460/ajvr.1995.56.01.51.
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SUMMARY Sequential histologic, immunologic, and virologic features of herpesvirus-induced keratitis were studied in 18 experimentally infected cats. Histologic changes were assessed by use of light microscopy, and the presence of viral antigen, B lymphocytes, and T lymphocytes was verified immunohistochemically. Flow cytometry was used to monitor changes in blood T lymphocytes (CD4 and CD8 homologues) and B lymphocytes. Cellular immunity was assessed by use of the lymphocyte proliferation assay. Development of stromal keratitis was preceded by prolonged absence of corneal epithelium, decreased numbers of circulating lymphocyte subsets, decreased mitogen responses, and acquisition of viral antigen by the corneal stroma. Return to normal of circulating lymphocyte numbers and function was temporally associated with the arrival of neutrophils and B and T lymphocytes in the corneal stroma. Sequelae to stromal inflammation were fibrosis and scarring. Findings suggest that suppression of local immune responses allows virus access to the corneal stroma, and that subsequent keratitis is mediated by an immune response to viral antigen.
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Ali, Mohamed, Harika Dasari, Virginia Van Keulen, Ashley Egan, Tobias Peikert, and Eva M. Carmona. "Microbial Activation of B-cells by Pattern Recognition Receptors Contributes to the Proinflammatory and Profibrotic Milieu in Patients with Idiopathic Pulmonary Fibrosis." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 190.20. http://dx.doi.org/10.4049/jimmunol.202.supp.190.20.
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Abstract We hypothesize that B-lymphocytes are conducive to the pathogenesis of idiopathic pulmonary fibrosis (IPF), a progressive and fatal interstitial lung disease. B-lymphocytes aggregate in the lungs of IPF patients to form tertiary lymphoid follicles. How these follicles are formed and their role in the pathogenesis of IPF is not known. Hence, we sought to characterize how the activation of B-lymphocytes from IPF patients may contribute to the disease. Methods IPF patients defined by ATS guidelines were identified and recruited under local IRB #14-004714. B-lymphocytes were then isolated by negative selection. Cytokines and immunoglobulins from plasma or B-lymphocyte supernatants were measured by ELISA and signaling pathways were elucidated from whole-cell lysates by immunoblotting. Our results show that B-lymphocyte aggregates are present within fibrotic areas of the lung of IPF patients and that activated B-lymphocytes induce fibroblast migration. This effect was abrogated by nintedanib inhibition of B-lymphocyte activation. Furthermore, microbial antigen (β-glucan and CpG) activation of B-lymphocytes through pattern recognition receptors (PRRs; TLR9 and Dectin-1) contributed to the proinflammatory and profibrotic milieu seen in IPF patients. Stimulation of TLR9 and Dectin-1 resulted in activation of mTOR-dependent and -independent pathways, respectively. Rapamycin decreased TLR9 signaling, but not Dectin-1 mediated pathways. Nintedanib abrogated B-cell activation, IgM production, and the profibrotic milieu by interfering with both the mTOR-dependent and -independent pathways. In conclusion, our findings implicate activated B-lymphocytes in IPF pathogenesis highlighting the role of PRRs in this disease.
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Tashireva, L. A., A. Yu Kalinchuk, T. S. Gerashchenko, O. E. Savelyeva, and V. M. Perelmuter. "Subpopulations of B lymphocytes in patients with breast cancer depending on the PD-L1 status." Bulletin of Siberian Medicine 22, no. 1 (April 20, 2023): 88–95. http://dx.doi.org/10.20538/1682-0363-2023-1-88-95.
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Aim. To study the association between the functional potency and degree of maturity of B lymphocytes and PD-L1 expression in breast cancer patients.Materials and methods. The study included 37 patients with the morphologically verified diagnosis of invasive breast cancer of no special type (IBC NST). The PD-L1 status was determined immunohistochemically using the Ventana SP142 assay (Roche, USA). Using the multiplex flow cytometry-based assay and high-throughput sequencing of the tumor microenvironment, subpopulations of B lymphocytes and their CD27 and PD1 expression profiles were determined, taking into account the PD-L1 status.Results. In the tumor microenvironment, regardless of the PD-L1 status, expression signatures of five lymphocyte subpopulations were determined. However, in PD-L1-positive patients, the levels of B lymphocytes and immunoglobulin class-switched B lymphocytes were higher compared with PD-L1-negative patients. Evaluation of the number of different B lymphocyte subpopulations by flow cytometry showed that PD-1-positive B lymphocytes predominated in the tumor microenvironment in PD-L1-positive patients, regardless of the degree of lymphocyte maturity.Conclusion. The results of the study showed predominance of mature committed B lymphocytes and memory B lymphocytes capable of synthesizing immunoglobulins of different classes and Th2 cytokines involved in type 2 immune response in PD-L-positive tumor microenvironment. It suggests that immunotherapy with PD-L1 inhibitors is highly likely to activate cells with protumor potential and can ultimately contribute to breast cancer progression.
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Grubeck-Loebenstein, B., H. Kassal, P. P. A. Smyth, K. Krisch, and W. Waldhäusl. "The prevalence of immunological abnormalities in endemic simple goitre." Acta Endocrinologica 113, no. 4 (December 1986): 508–13. http://dx.doi.org/10.1530/acta.0.1130508.
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Abstract. Thyroid growth stimulating immunoglobulins microsomal antibodies and antibodies against thyroglobulin were determined in patients with simple goitre (n = 20) and controls (n = 6) living in an iodine deficient area. In addition, lymphocytic infiltration of thyroid tissue, the amount of the various lymphocyte subsets (Leu 4+, Leu 3a+, and Leu 2a+ T-cells as well as B1+ B cells) in the thyroid gland, as well as the expression of the histocompatibility antigen HLA-DR on thyrocytes and intrathyroidal T-lymphocytes were examined. Goitrous patients were subdivided into two groups according to their individual iodine supply estimated by iodine excretion values, and immunological parameters were compared between patients with low (group A, iodine excretion < 70 μg/24 h) and with higher (group B, iodine excretion> 100 μg/24 h) iodine supply. Thyroid growth stimulating immunoglobulins and antithyroid antibodies were equally prevalent in the two patient groups, but were absent in controls. Lymphocytic infiltration of thyroid tissue was present to a comparable extent in patients of groups A and B, but to a distinctly lower degree in control persons. Intrathyroidal T-lymphocyte subsets did not differ between patients and controls. B-lymphocytes, germinal centres as well as DR+ thyrocytes were detected in goitrous patients of both groups, but never in control persons. Thus, immunological abnormalities frequently occur in patients with simple goitre and do not depend upon individual iodine supply.
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Ueda, Yoshihiro, Kaiyong Yang, Sandra J. Foster, Motonari Kondo, and Garnett Kelsoe. "Inflammation Controls B Lymphopoiesis by Regulating Chemokine CXCL12 Expression." Journal of Experimental Medicine 199, no. 1 (January 5, 2004): 47–58. http://dx.doi.org/10.1084/jem.20031104.
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Inflammation removes developing and mature lymphocytes from the bone marrow (BM) and induces the appearance of developing B cells in the spleen. BM granulocyte numbers increase after lymphocyte reductions to support a reactive granulocytosis. Here, we demonstrate that inflammation, acting primarily through tumor necrosis factor α (TNFα), mobilizes BM lymphocytes. Mobilization reflects a reduced CXCL12 message and protein in BM and changes to the BM environment that prevents homing by cells from naive donors. The effects of TNFα are potentiated by interleukin 1 β (IL-1β), which acts primarily to expand the BM granulocyte compartment. Our observations indicate that inflammation induces lymphocyte mobilization by suppressing CXCL12 retention signals in BM, which, in turn, increases the ability of IL-1β to expand the BM granulocyte compartment. Consistent with this idea, lymphocyte mobilization and a modest expansion of BM granulocyte numbers follow injections of pertussis toxin. We propose that TNFα and IL-1β transiently specialize the BM to support acute granulocytic responses and consequently promote extramedullary lymphopoiesis.
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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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Wang, Hairong, Cheng-Cheng Guo, Hongyu Chen, Yang Qun-ying, and Zhong-ping Chen. "IMMU-49. DYNAMIC CHANGES AND PROGNOSTIC VALUE OF PERIPHERAL BLOOD LYMPHOCYTE SUBSETS IN INTRACRANIAL GERM CELL TUMORS." Neuro-Oncology 23, Supplement_6 (November 2, 2021): vi103—vi104. http://dx.doi.org/10.1093/neuonc/noab196.408.
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Abstract OBJECTIVE This study was designed to retrospectively analyze the dynamic changes of peripheral blood lymphocyte subsets and prognosis among patients with intracranial germ cell tumors. METHODS A total of 150 intracranial germ cell tumors patients diagnosed between June 2011 till November 2019 were retrospectively investigated. Peripheral blood total T lymphocytes (CD3+) percentage, T helper/inducible lymphocytes(CD3+CD4+)percentage, T inhibitory/toxic lymphocytes (CD3+CD8+) percentage, B lymphocyte (CD19+) percentage, NK lymphocyte (CD3/CD16+CD56+) percentage, regulatory T cells (CD4+CD25+,CD8+CD25+), and T helper/toxic lymphocyte ratio (CD4+/CD8+ ratio) were quantified by flow cytometry analysis. Clinical information was extracted from the database in Sun Yat-sen University Cancer Center and survival data was confirmed through outpatient visits and telephone follow-up. RESULTS T lymphocytes population was increased after anti-tumor treatment, with significant difference of total T lymphocytes (CD3+), inhibitory/toxic T cells (CD3+CD8+) and regulatory T cells (CD4+CD25+ and CD8+CD25+), (p=0.008, p=0.000, p=0.008 and p=0.001 respectively), while B lymphocytes(CD19+) decreased after chemotherapy(p=0.003). The dynamic levels of T lymphocyte and B lymphocyte subpopulation after chemotherapy did not present significant differences between gender, age, and locations of tumors (p >0.05), except CD4+CD25+ T cells in younger children (age< 16 years older) increased significantly than the elder (age >16), p=0.04. Patients with increased CD19+ B cells presented significant suboptimal outcomes compared with the no increased (p=0.024). Similarly, increased CD3+ T cells, CD3+CD8+ T cells, CD4+CD25+ T cells reduced the risk of death (p=0.006, p=0.019, p=0.042 respectively). Multivariate Cox Regression analysis showed: increased CD19+ B cells, p=0.04, HR=1.688, 95%CI=1.025-2.779. CONCLUSION After anti-tumor treatment, cell-mediated immunity activated, enhanced, and dominated in anti-tumor response. An increased level of CD19+ subsets was an independent predictor for inferior overall survival. Systemic circulating T cells immunity played an important role and mediating antitumor responses may pave the road for new immunity strategies.
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Tang, Mimi L. K., Douglas A. Steeber, Xiu-Qin Zhang, and Thomas F. Tedder. "Intrinsic Differences in L-Selectin Expression Levels Affect T and B Lymphocyte Subset-Specific Recirculation Pathways." Journal of Immunology 160, no. 10 (May 15, 1998): 5113–21. http://dx.doi.org/10.4049/jimmunol.160.10.5113.
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Abstract Lymphocyte migration into lymphoid organs is regulated by tissue-specific adhesion molecules such as L-selectin and the α4β7 integrin. Whether L-selectin also regulates lymphocyte subset-specific migration into specific lymphoid tissues was examined in this study by comparing the migration of CD4+ T cells, CD8+ T cells, and B cells from L-selectin-deficient and wild-type mice. T cells were the predominant lymphocyte subset entering PLN, MLN, Peyer’s patches, and spleen during short term (1-h) migration assays. However, both B cell and CD4+ and CD8+ T cell entries into PLN, MLN, and Peyer’s patches were dramatically impaired (73–98%) by loss of L-selectin. Lymphocyte expression of α4β7 integrin did not compensate for the loss of L-selectin, since both B and T cells predominantly migrated into the spleen in the absence of L-selectin. The more efficient migration of T cells into peripheral lymphoid tissues relative to that of B cells was partly explained by the finding that T cells expressed L-selectin at 50 to 100% higher levels than B cells. In addition, a 50% reduction in L-selectin expression by lymphocytes from hemizygous L-selectin+/− mice resulted in a 50 to 70% decrease in short term lymphocyte migration into peripheral lymphoid tissues relative to that of wild-type lymphocytes. Thus, the differential migration of T and B lymphocyte subsets to lymphoid tissues is regulated in part by subset-specific differences in L-selectin expression levels.
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Levitt, D., and R. Danen. "Development and regulation of chlamydia-responsive murine B lymphocytes." Journal of Immunology 138, no. 10 (May 15, 1987): 3468–74. http://dx.doi.org/10.4049/jimmunol.138.10.3468.
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Abstract We have examined characteristics of chlamydia-stimulated mouse B cells as well as cells that regulate polyclonal responses in vitro. B lymphocyte proliferation stimulated by chlamydia arises at a similar time as Escherichia coli lipopolysaccharide (LPS)-induced proliferative responses during ontogeny. In contrast, development of immunoglobulin (Ig)-secreting cells after chlamydia stimulation is delayed by several weeks relative to ontogeny of LPS-inducible plaque-forming cells (PFC). The lack of Ig secretion by immature B cells is not due to a deficiency of Lyb5+ B lymphocytes, since X-linked immunodeficient (xid) NBF1 mice that lack this B lymphocyte population respond well to chlamydia stimulation. Adherent cells are important for chlamydia-stimulated B lymphocyte differentiation, but are not as necessary for their proliferation. Neither adult adherent cells nor T cells can correct the inability of immature spleen cells to develop into Ig-secreting cells; spleen cells from 2-wk-old mice (i.e., immature B cells) will not suppress adult B lymphocyte responses to chlamydia. When B lymphocytes are separated according to their buoyant densities, chlamydia stimulates low density (activated) B cells to proliferate and differentiate better than high density (resting) cells. Proliferative responses to chlamydia arise earlier during ontogeny, do not require adherent cells, and can proceed to a relatively greater extent in resting B cell population (compared with activated B cells) than induction of Ig-secreting cells.