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Query: UMLS:C0079731 (B-cell lymphoma)
 16,671 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Endopeptidase activity was characterized in plasma membranes prepared from an antigen-presenting B cell lymphoma, A20. Activity was detected at both neutral and acid pH, and studies with inhibitors confirmed that a number of different enzymes, most probably cysteine, metallo, and aspartic endopeptidases, were associated with the A20 cell surface.
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PMID:Endopeptidase activities associated with the plasma membrane compartment of an antigen-presenting B cell. 253 76

Cross-linking of membrane IgG2a or IgD on the B cell lymphoma A20.1 resulted in the elaboration of lymphokines which were able to support the growth of HT-2 cells and to induce increased Ia expression on resting B cells. Unstimulated A20.1 cell did not produce detectable levels of lymphokine activity. Lymphokine secretion did not occur in response to cross-linking of MHC class II (Ia) or class I (H2K) molecules. The kinetics for secretion were rapid, with detectable levels of lymphokine arising within 3 to 4 h of stimulation. Maximal lymphokine production was reached by 8 to 10 h. Soluble intact anti-Ig antibodies failed to stimulate lymphokine production due to Fc-mediated effects. This was concluded based on the fact that soluble F(ab')2 fragments of anti-IgG, but not soluble intact antibody, stimulated the production of lymphokine by A20.1 cells. Based on serologic criteria, membrane Ig cross-linking by ligand induced secretion of IL-2 but not IL-4 by A20.1 cells. Induction of Ia expression by resting B cells in response to A20.1 supernatant was not mimicked by stimulation with IL-1, -3, -5, or -6 either singly or in combination. Furthermore, preliminary physicochemical characterization revealed that the Ia-inducing factor in A20.1 supernatant has a molecular weight greater than 50,000. These data suggest that the Ia-inducing activity is a novel lymphokine. Thus, this report describes the first evidence for the existence of a B cell tropic lymphokine produced by B cells in response to Ag receptor-mediated signal transduction.
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PMID:Production of multiple lymphokines by the A20.1 B cell lymphoma after cross-linking of membrane Ig by immobilized anti-Ig. 266 89

T cell hybridomas with specificity for VSV (vesicular stomatitis virus)-infected cells were generated in an attempt to better define the la-restricted helper T cell response to VSV. The hybridomas were created by fusing BALB/c (H-2d) anti-VSV immune spleen cells to the murine thymoma BW 5147. These hybridomas produce IL-2 when stimulated with VSV-infected spleen cells. They were found to recognize viral antigens in association with I-Ad and, in addition, could also be stimulated by VSV-infected A20 cells (an Ia-positive B cell lymphoma of H-2d origin). The purified viral membrane glycoprotein, G protein, and Gs (secreted G protein that lacks the hydrophobic and intracytoplasmic domains) both stimulated IL-2 production when added to cultures of A20 and the hybridomas. These hybridomas therefore recognize a viral antigenic determinant on G protein. Since chemically-fixed antigen-presenting cells fail to stimulate the hybridomas after exogenous addition of purified G protein we can conclude that these T cell hybridomas recognize a processed form of the G protein. Stimulator cells created by expression in A20 of a transfected cDNA encoding G protein were also recognized. Recognition in this case was I-Ad-restricted, as anti-I-Ad monoclonal antibodies blocked stimulation, and an Ia-negative cell (P815) expressing a transfected G protein gene failed to stimulate the hybridomas. Even after paraformaldehyde fixation, G gene-transfected, Ia-positive cells could stimulate the hybridomas, suggesting that processing of this endogenously-synthesized antigen has occurred.
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PMID:T cell hybridomas define the class II MHC-restricted response to vesicular stomatitis virus infection. 285 79

In order to investigate T cell-B cell interactions we constructed monoclonal, antigen-specific T- and B-cell populations. The Ia+ B-cell lymphoma A20-2J was transfected with trinitrophenyl (TNP)-specific heavy (mu) and light (kappa) chain Ig genes. A hapten-carrier complex (TNP-keyhole limpet hemocyanin (KLH)) bound to the surface Ig expressed on the transfectant and was presented to carrier-specific T-cell hybridoma clones at markedly low doses of antigen (0.01 microgram/ml) and in an Ia-restricted fashion. Two responses were elicited in the responding T-cell clones: (i) high levels of IL-2 secretion (320 units/ml), and (ii) cytotoxicity directed against the antigen-presenting B cell. This cytotoxicity was inhibited by D-mannose and was directed against innocent bystander cells, unlike cytotoxicity mediated by NK cells or alloreactive cytotoxic T lymphocyte. Helper and cytotoxic functions were often present in different T-cell hybridomas but some clones exhibited both activities. One representative T-cell hybridoma exhibited strong helper function for TNP-primed splenic B cells as detected in a plaque-forming cell assay, but was cytotoxic toward antigen-presenting B cells. Such monoclonal assay systems for studying cognate interactions of heterogeneous T cells and specific antigen-presenting cells will provide us with valuable new approaches for the study of antigen-specific T-cell regulation of B-cell activation in immune responses.
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PMID:Clonal analysis of antigen-specific interactions between T cells and genetically engineered B cells. 295 69

Supernatants containing lymphotoxin (LT) and immune interferon (IFN-gamma) or IFN-gamma alone were produced by antigen-stimulated murine T cell clones. These lymphokine preparations as well as cloned recombinant murine IFN-gamma (Genentech) were tested for antiproliferative activity on a variety of murine T, B, macrophage, and mastocytoma tumors and on T cell clones and LPS-stimulated B cells. The growth of every cell line tested was susceptible to the LT-containing supernatants. Cloned recombinant murine IFN-gamma inhibited the growth of A9 fibroblasts but not L929 cells. Neither the cloned murine IFN-gamma nor that produced by a T cell clone had any appreciable effect on the lymphoid cells except for one B cell lymphoma, A20. The sensitivity of nontransformed T and B cells to LT indicates that this lymphokine may play an immunoregulatory role. Indeed, the T cells that produce LT are sensitive to its cytotoxic activity and, therefore, regulate themselves. The differential inhibitory effects of LT and IFN-gamma on lymphoid target cells allow us to distinguish between preparations that contain IFN-gamma alone and those that contain LT and IFN-gamma. The susceptibility of lymphoid tumors to the antiproliferative activity of the LT-containing preparations indicates that LT either alone or together with IFN-gamma may be useful in tumor therapy.
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PMID:The differential inhibitory effect of lymphotoxin and immune interferon on normal and malignant lymphoid cells. 298 82

A B cell lymphoma A20.2J and splenic B cells produced an active material to support the proliferation of an interleukin 2 (IL-2)-dependent T cell line, CTLL-2, by stimulation with both calcium ionophore A23187 and phorbol myristate acetate (PMA). Although the production of the active material was induced by stimulation with A23187 alone in A20.2J cells, both A23187 and PMA were essential for the stimulation of splenic B cells. Neither A20.2J cells nor splenic B cells produced the active material by stimulation with PMA alone. The production was inversely proportional to the concentration of fetal calf serum in culture medium. The active material produced by B cells was indicated to be IL-2 and not B cell-stimulating factor 1 (BSF-1) for the following reasons: 1) the proliferation of CTLL-2 cells in the presence of active material was inhibited by the inclusion of anti-IL-2 receptor or anti-IL-2 in culture medium but not by anti-BSF-1; 2) the material showed no co-mitogenic activity to purified splenic B cells with anti-immunoglobulins and did not support the proliferation of FDC-P2 which are known to grow in the presence of BSF-1; and 3) IL-2 mRNA could be detected in A20.2J and splenic B cells stimulated with A23187 and PMA in Northern blot analysis. Some B cell hybridomas were also shown to produce IL-2 by similar stimulation to A20.2J. Splenic B cells as well as A20.2J cells were able to produce IL-2 by stimulation with anti-immunoglobulins. These results suggest that under certain conditions IL-2 can be produced by splenic B cells, at least some subsets of B cells, and B cell lines.
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PMID:Interleukin secretion by B cell lines and splenic B cells stimulated with calcium ionophore and phorbol ester. 311 82

We examined the ability of a set of cloned chicken ovalbumin (cOVA)-specific, Id-restricted, T cell hybridomas to produce interleukin-2 in response to cOVA presented by the Ia+ B cell lymphoma line, A20-2J. Although viable A20-2J cells presented native, denatured, and fragmented cOVA more or less equally well, A20-2J cells that were glutaraldehyde-fixed could present only enzymatically or chemically fragmented cOVA. These results suggest that antigen fragmentation may be both necessary and sufficient to define accessory cell processing of soluble antigens so that they may be recognized in association with I-region molecules by T cells.
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PMID:Antigen recognition by H-2-restricted T cells. I. Cell-free antigen processing. 619 18

Stimulation of B lymphocytes by the cross-linking of surface Ig (sIg) with an F(ab')2 antibody fragment leads to the rapid activation of several tyrosine kinases. This gives rise to the activation of phospholipase C gamma (PLC gamma) and the generation of inositol phosphates. These, in turn, lead to a prolonged elevation of intracellular Ca2+ ([Ca2+]i) consisting of a rapid release of Ca2+ from intracellular stores and a sustained influx of extracellular Ca2+. In contrast, co-cross-linking sIg to Fc gamma receptor (Fc gamma RII) with intact anti-sIg induces a much more transient increase in [Ca2+]i. Stimulation of the murine B cell lymphoma, A20, with F(ab')2 anti-sIgG leads to the production of high levels of IL-2, while co-cross-linking of sIgG with Fc gamma RII blocks this response. In studies reported here, we show that co-cross-linking of Fc gamma RII with sIg prevents the influx of extracellular Ca2+ without significantly affecting the tyrosine phosphorylation of substrates including PLC gamma 1, PLC gamma 2, and Syk or the mobilization of Ca2+ from intracellular stores. In cells that had been previously activated with F(ab')2 anti-IgG, co-cross-linking of sIg to Fc gamma RII rapidly abrogated the influx of extracellular Ca2+ by closing the plasma membrane Ca2+ channel. Additionally, even 2-3 h after stimulation of the cells with F(ab')2 fragment, addition of intact anti-IgG to the cells, or removal of extracellular Ca2+, markedly inhibited (> 90%) IL-2 production. These results indicate that co-cross-linking sIg with Fc gamma RII both prevented the opening of and actively closed the Ca2+ channel, and, through this mechanism, Fc gamma RII was able to control production of IL-2. Overall, since influx of extracellular Ca2+ has been found to be necessary for the proliferation and differentiation of B cells, Fc gamma RII may play a critical role in controlling these responses by regulating the opening of the Ca2+ channel.
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PMID:Cross-linking of Fc gamma receptor to surface immunoglobulin on B cells provides an inhibitory signal that closes the plasma membrane calcium channel. 751 64

In human T cells CD45 is reported to associate with both cell surface and intracellular molecules including CD2, CD4/CD8, CD5, p56lck and p59fyn. In this study the association of molecules with CD45 in murine T lymphocytes was explored using biotinylation, chemical cross-linking, immunoprecipitation and 32P-labelling. Sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE) analysis of CD45 monoclonal antibody (mAb) (S-450-15.2) immunoprecipitates from Triton X-100 lysates of murine thymocytes that were surface biotinylated and treated with the chemical cross-linker 3,3'-dithio-bis(sulpho-succinimidylpropionate) (DTSSP) showed that CD45 can be chemically linked to molecules of 25,000-32,000, 42,000 and 60,000-70,000 MW. The CD45 mAb also co-precipitated a prominent 32,000 MW molecule from digitonin lysates of surface biotinylated murine thymocytes, splenocytes and D10 cells, but a weaker association was also detected on splenic B cells and on the murine B-cell lymphoma line A20. The results suggest that in these cells CD45 is associated with a 32,000 MW molecule which is exposed extracellularly. Experiments in which thymocytes were biotinylated after permeabilization with lysolecithin showed that additional molecules of 33,000, 55,000, 60,000 and 90,000 MW, presumably localized intracellularly, also co-precipitated with CD45. Labelling of murine thymocytes or D10 cells with H3(32)PO4 in vivo, and of CD45 immunoprecipitates by in vitro kinase reaction, revealed that the 32,000-33,000 MW molecules are phosphoproteins. The relationship of these molecules with the 30,000-34,000 MW molecules previously reported to associate with CD45 in human T cells is not clear as a number of differences were observed. Firstly, the molecular weight of the CD45-associated 32,000-33,000 MW molecule(s) on murine T cells and B cells is slightly lower than that observed in the human T-cell line Jurkat (34,000 MW). Secondly, phosphoamino acid analysis after in vitro kinase labelling of CD45 immunoprecipitates showed that the murine 32,000-33,000 MW molecules are phosphorylated exclusively on serines. Thirdly, although in vitro phosphorylation of the 32,000-33,000 MW molecules was inhibited by preincubation with either GTP-gamma-S or GDP-beta-S, the 32,000-33,000 MW CD45-associated molecules did not bind 32P-GTP, GDP-agarose, or react with antisera to a consensus sequence of G proteins. The crucial role of CD45 for proper function of the T-cell receptor (TCR), suggests that the CD45-associated 32,000-33,000 MW molecules and kinases also may play a role in the signalling events leading to T-cell activation.
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PMID:Evidence for an association of CD45 with 32,000-33,000 MW phosphoproteins on murine T and B lymphocytes. 783 67

beta-Endorphin affects mononuclear cell proliferation, cytokine production and calcium uptake in a naloxone-resistant manner. The presence of naloxone-insensitive binding sites for beta-endorphin have been demonstrated on murine EL4-thymoma cells, transformed human mononuclear cells and normal murine splenocytes. Since murine splenic B cells have been shown to express naloxone-resistant receptors for beta-endorphin in response to the mitogen, concanavalin A (Con A), the A20 B-cell lymphoma line was used to further study regulation of this site by Con A and dexamethasone. Analyses showed two sites: a high-affinity site, Kd1 = (8.7 +/- 2.3) x 10(-11) M and binding capacity (Bmax1) of (2.6 +/- 2.0) x 10(3) receptors/cell; and a low-affinity site, Kd2 = (2.2 +/- 0.8) x 10(-8) M with Bmax2 of (1.5 +/- 0.8) x 10(5) receptors/cell. Competition studies showed that N-acetyl-beta-endorphin was approx. 5-fold and beta-endorphin6-31 10-fold less potent than beta-endorphin1-31. Neither beta-endorphin1-27 nor naloxone, morphine or other opioid receptor agonists displaced [125I]beta-endorphin. Con A (20 micrograms/ml) significantly increased the Bmax (3.5-fold; expressed per cell) and resulted in a loss of the higher-affinity site. However, the increased Bmax occurred in proportion to the Con-A-induced increase in protein/cell. Dexamethasone (Dex) also increased Bmax, primarily by increasing (2-3-fold) the number of lower affinity sites. In contrast to Con A, two binding sites persisted after treatment with Dex, which exerted a minimal effect on protein/cell. Therefore, binding/cell and binding/protein/cell were both significantly enhanced by Dex. The combined effects of Dex and Con A on binding failed to show additivity or synergy. When binding was analyzed per protein/cell, the effect of Con A appeared to dominate; the Dex-enhanced binding/protein/cell was no longer evident in the presence of Dex plus Con A. Thus, Dex and Con A may enhance binding by independent mechanisms.
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PMID:Expression of naloxone-resistant beta-endorphin binding sites on A20 cells: effects of concanavalin A and dexamethasone. 785 49


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