Viewing affirmative mentions of negative regulation of IL2 (H. sapiens) in B cells

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Antonaci et al. (1989)interleukin 2B cellThe suppressive factors are also responsible for a decreased interleukin 2 (IL-2) synthesis since a similar pretreatment of cell suspensions or exogenous human IL-1 and/or IL-2 supplementation of aged cell cultures leads to a recovery of T regulatory effects on B cell differentiation.
Tao et al. (1991)IL-2B cellsT2 at 0.1-1 micrograms/ml inhibited antigen- and mitogen-stimulated proliferation of T cells and B cells, interleukin-2 (IL-2) production by T cells, and immunoglobulin production by B cells.
Kierszenbaum et al. (1991)interleukin-2B lymphocytesTrypanosoma cruzi induces suppression of DNA synthesis and inhibits expression of interleukin-2 receptors by stimulated human B lymphocytes.
Kierszenbaum et al. (1991)IL-2B-cellThese results demonstrate for the first time that T. cruzi can affect human B-cell responses and that the mechanism involves inhibition of IL-2 receptor expression.
Murakami et al. (1988)IL2B cellsSimilar suppression of IL2 and IgM production was observed in cultures of B cells and T4+ cells.
Tomita et al. (1990)IL-2B cellThis factor modulates the function of CD4+ cells suppressing their IL-2 production and suppressing PWM-induced B cell differentiation into Ig producing cells.
Manolagas et al. (1985)interleukin-2B lymphocytesIn addition 1,25(OH)2D3 is a potent inhibitor of interleukin-2 (IL-2) and suppresses effector functions of both T and B lymphocytes via IL-2-dependent as well as via IL-2-independent mechanisms.
Parker (1982)IL 2B cellsPartial removal of IL 2 results in partial removal of helper activity for B cells.
Ayanlar-Batuman et al. (1986)interleukin-2B cellDefective interleukin-2 production and responsiveness by T cells in patients with chronic lymphocytic leukemia of B cell variety.
Steinberger et al. (1996)IL2B cellsMoreover, a control protein lacking IL2 as the targeting moiety of the chimera had no effect toward all B cells tested, thus establishing its specific activity.
Cunningham-Rundles et al. (1995)IL-2B cellAlthough there appear to be intrinsic B cell defects, many have poor T cell proliferation and deficient secretion of IL-2, IL-4, IL-5 interferon-gamma, and B cell differentiation factor.
Lê thi Bich-Thuy and Fauci (1985)interleukin 2B cellsDirect effect of interleukin 2 on the differentiation of human B cells which have not been preactivated in vitro.
Thompson et al. (1987)IL2B-lymphocytesThe lymphopenia was nonselective; T- and B-lymphocytes decreased in an IL2 dose-dependent manner, without consistent change in the OKT4:OKT8 ratio.
Drexler et al. (1988)IL-2B cellsOur data suggest that (a) B-CLL cells are able to respond to direct stimulation of the second messenger pathway (through protein kinase C) but not to the physiological stimuli IL-2 or BCDF; (b) the defect in signal transduction appears to be located upstream of protein kinase C (a possible candidate is a G protein); (c) malignant B cells may spontaneously or after treatment with inducers express the IL-2 receptor (Tac antigen) in the absence of a functional differentiating response to IL-2; and (d) signs of proliferation/differentiation in B-CLL samples after incubation with IL-2 or BCDF might be due to contamination of the cell populations with residual normal B cells.
Kindler et al. (1995)IL-2B lymphocytesLower IL-2 expression (detected only as mRNA synthesis) was also induced in the cultured B lymphocytes after incubation with cross-linking anti-IgM antibodies instead of PMA plus ionomycin.
Nakagawa et al. (1986)interleukin 2B cellSequential synergistic effect of interleukin 2 and interferon-gamma on the differentiation of a Tac-antigen-positive B cell line.
Holen and Elsayed (1998)IL-2B cellsHigh IgE secretion, from 1% remaining B cells in one of the patients, following PHA+IL-2 stimulation, could be reduced by the drugs.
Jego et al. (2001)IL-2B cellsCD25 (IL-2Ralpha) was increased 72 +/- 10-fold on activated B cells, but decreased and then disappeared on plasmablasts.
Vazquez et al. (1991)interleukin 2B cellDifferential inhibition of interleukin 2- and interleukin 4-mediated human B cell proliferation by ionomycin: a possible regulatory role for apoptosis.
Kolb et al. (1993)IL-2B cellTaken together, these observations indicate that IL-2 and IL-4 use different signaling pathways to induce the G1-->S transition in these cells and suggest that the IL-4 inhibition of the B cell response to IL-2 may result from its effect on cAMP generation.
Ceuppens and Stevens (1986)IL-2B cellsWe conclude that IL-2 acts on PWM-activated B cells in conjunction with other helper factors to induce Ig production and that anti-Tac inhibits PWM-induced Ig production by blocking IL-2 receptors on activated B cells.
Carosella et al. (1989)IL-2B cellThis work explores the roles of interleukin 1 (IL-1) and interleukin 2 (IL-2) in B cell differentiation induced by Fc fragments.
Yoshimura et al. (1989)IL-2B cellInhibition of the production of IL-2 and gamma-IFN, but not B cell-stimulating factor 2.
Hashimoto et al. (1986)IL2B cellsThe following results were obtained: (a) B cells activated with LPS plus anti-Ig were found to proliferate in response to either recombinant IL2, T cell SN or fresh LPS; (b) a monoclonal anti-IL2 receptor antibody (PC61) could completely inhibit the effects of recombinant IL2 or various T cell SN (cloned T helper cell SN, EL4 SN, concanavalin A-spleen cell SN or mixed leukocyte culture SN), but did not interfere with the effect of LPS; (c) B cells activated with LPS or LPS plus anti-Ig were not found to secrete detectable amounts of IL2 by themselves.
Perri and Kay (1987)IL-2B cellsThe proliferative response of control and CLL B cells to both a partially purified preparation of IL-2 and recombinant IL-2 (rIL-2) was also examined.
Miller (1997)interleukin-2B lymphocytesCyclosporine A suppresses production of interleukin-2, a cytokine necessary for the amplification stages of the immune response and critical for the activation of both T and B lymphocytes.
Maher et al. (1990)IL-2-inducedB cellsMitogen-induced pre-activation of B cells in the presence of IL-4 resulted in a reduction in subsequent IL-2-induced IgM secretion without significantly affecting proliferation.
Maher et al. (1990)IL-2B-cellHuman B-cell tumours were also cultured over a 2-3 day period in the presence of anti-Ig beads plus IL-2, or IL-4 or both IL-2 and IL-4.
Nonoyama et al. (1994)IL-2B cellsThe addition of IL-2 also increased immunoglobulin synthesis by anti-CD40/IL-10-activated B cells from patients with common variable immunodeficiency (CVI) and defective IL-2 production, suggesting that in a subgroup of CVI patients the IL-2 deficiency may contribute to the observed hypogammaglobulinemia.
Lee et al. (1990)IL-2B cellsThese data suggest that IL-4 has a capacity to block the up-regulation of the high as well as low affinity IL-2R-induced by IL-2 in normal human B cells, and could provide a possible explanation for the decreased responsiveness of B cells to IL-2 in the presence of IL-4.
Doi et al. (1988)IL-2B-cellMononuclear cells (MNC) of the patient showed no proliferative response (stimulation index, less than 2) to T-cell mitogens (PHA and Con A) and were defective in IL-2 production and IL-2R expression (less than 1%), whereas productions of other lymphokines (B-cell differentiation factor and IFN-gamma) were not impaired significantly.
Hirohata (1992)IL2B cellsAlthough CCA suppressed IL2 production by immobilized anti-CD3 activated CD4+ T cells, its suppressive effects on B cells were not overcome by the addition of IL2 or factors generated from mitogen activated T cells (TF).
Foa et al. (1985)IL 2B cellsHowever, the titer of IL 2 was greatly reduced when autologous leukemic B cells were added to the culture system.
de Totero et al. (1994)IL2B-cellTaken together, it is suggested that the expression of IL2 receptors is up- or down-regulated during the process of B-cell lineage activation and differentiation.
Bartlett et al. (1989)lymphokineB cellIn order to determine the involvement of T-B cell contact vs lymphokine production in mediating B cell cycle entry and progression, Th cell clones "defective" in lymphokine production were cloned.
Sayed-Noor (2009)interleukin-2B-cellsFurther advancement was achieved by the discovery and the use of agents such as Tacrolimus which inhibits T-lymphocyte signal transduction and interleukin-2 transcription, and Sirolimus which inhibits the response to interleukin-2 thereby blocking the activation of T- and B-cells.
Tangye and Raison (1997)IL-2B cellsInterestingly, the ability to suppress apoptosis in leukaemic CD5+ B cells was also found to be a property of IL-2, IL-6, IL-13 and TNF-alpha.
Kasprzak et al. (2010)IL-2B-cellAs compared with non-neoplastic lesions, in B-cell NHLs a significantly higher expression was noted of both IL-2 and IL-22R(alpha).
Kasprzak et al. (2010)IL-2B-cellUsing hybridocytochemistry, presence of mRNA for IL-2 could be detected, but not mRNA for IL-22R(alpha) in children with B-cell NHLs.
Chen et al. (1987)IL-2B cellAddition of in vitro purified IL-1 to nonadherent cells enhanced 1,25-dihydroxyvitamin D3-induced inhibition of Ig production. 1,25-Dihydroxyvitamin D3 also inhibited the expression of IL-2 receptors on B cells activated with SAC. 1,25-dihydroxyvitamin D3 did not inhibit Ig production by SAC preactivated B cell blasts in response to T cell supernatants.
Chen et al. (1987)IL-2B cellsThese data suggest that vitamin D3 inhibits Ig production by inhibiting IL-2 receptor expression on B cells and via its effect on adherent macrophages.
Schena et al. (1992)IL-2B cellsIL-2 production is limited to the actively proliferating GC-B blasts, IL-1 beta and IL-6 to resting M-B cells.
Faist et al. (1996)interleukin 2B cellPGE2 is an inhibitor of T cell mitogenesis, interleukin 2 (IL-2) production, and IL-2 receptor expression; and it has a massive impact on the quality of B cell antibody synthesis.
Zhang et al. (1990)IL-2B cellsThe PMA-inducible helper activity was CsA-sensitive at the same CsA concentration that inhibited IL-2 secretion of EL-4 cells, but the murine factors in EL-4 supernatant had no effect on human B cells; the helper effect did not occur across a semipermeable membrane.
Perri (1986)B cell growth factorB cellsImpaired expression of cell surface receptors for B cell growth factor by chronic lymphocytic leukemia B cells.
Benjamin et al. (1986)IL-2B lymphocytesSince some Burkitt's lymphoma lines express Tac antigen and can be triggered to secrete IL-2 following activation with the new tumor promoter teleocidin, we addressed the question of whether the induction of IL-2 by B lymphocytes is accompanied by the induction of IFN-gamma.
Rapaport et al. (1991)interleukin-2B cellsTreatment resulted in a decrease in % B cells and in % T total cells and also decreases in most individual patients' mitogen responses and interleukin-2 receptor levels.
Jeong et al. (1986)IL-2B-cellDex did not induce IL-2 production and inhibited IL-2 production induced by Con A, in contrast to the promoting effects of Dex on BIF production, providing further evidence for the independence of BIF and IL-2 production and B-cell stimulation.
Sindhi et al. (2003)IL-2B-cellRESULTS: PD analyses suggested that in NHS samples containing CsA+SRL (n=5), (1) PMA-Ionomycin-stimulated T-cell expression of intracellular IL-2, TNF-alpha, and IFN-gamma was inhibited by CsA, and minimally by SRL, and (2) the two agents inhibited pokeweed mitogen (PWM)-stimulated B-cell expression of CD54 and CD95, but not CD86 (ICAM-1, Fas antigen, and B7.2), synergistically.
Fahlman et al. (1995)B cell growth factorB cellB cell growth factor were also inhibited by RA.
Dziedzic et al. (2004)IL-2B-cellAlterations in host defence mechanisms after trauma that are potentially important to development of infectious complications include the following: paralysis of monocyte function (transient nonreactivity of monocytes toward stimulation with endotoxin, depression of antigen presentation capacity, and enhanced secretion of the anti-inflammatory cytokine IL-10); suppression of T cell functions (decreased response to mitogenic activation and decreased IL-2 production); and impairment of B-cell function (decreased capacity to produce antibodies).
Nakagawa et al. (1987)IL 2B cellRecently, we reported that CsA (1 microgram/ml) inhibited PWM-induced T cell production of IL 2 and IFN-gamma, but supernatants retained B cell differentiation factor (BCDF)-like activity.
Kubota and Nakazato (1994)IL-2B-cellThe proliferation-suppressed hybrid lines exhibited phenotypic changes as follows: the usually high levels in YACUT of J11d antigen, IL-2 receptor, and c-myb expression, which are markers of immature T cells, were all down-regulated; the G4 T-cell function, i.e., contact helper activity for B-cell proliferation in T/B cell collaboration, was retained.
Benenson et al. (1986)lymphokineB-cellsAt the same time the use of the drug resulted in an elevation of the level of T-suppressors, a decrease in the amount of B-cells, T-helpers, titers of the rheumatoid factor, antisynovial antibodies, cytopathic and lymphokine synthesizing activity.
Soppi et al. (1985)lymphokineB-cellThe characterization of the patient's immunologic capacity disclosed practically normal T-cell number and mitogenic responses but impaired lymphokine production as well as B-cell function.
Oka et al. (1992)interleukin-2B-cellRESULTS: Patients with Barrett's esophagus had a significant suppression of all T-cell (p less than 0.01) and B-cell function (p less than 0.01) and interleukin-2 production (p less than 0.001) when they were compared to the controls.
Benjamin et al. (1989)IL-2B cellThe following similarities in the functional biological characteristics of T cell and B cell IL-2 suggest that B cell IL-2 is not a factor which mimics IL-2 activity in the CTLL-2 assay: (i) neutralization of IL-2 by anti-IL-2 monoclonal antibody (DMS-1); (ii) elution of IL-2 following its adsorption to CTLL-2 cells; (iii) determination of the MW of IL-2 by SDS-PAGE and Western blot analysis; and (iv) ability of B cell IL-2 to support T cell proliferation and blocking of this activity by anti-tac monoclonal antibody. cDNA probes for T cell IL-2, however, did not detect IL-2 mRNA in B cells.
Fevrier (1985)IL2B cellThese molecules alter T cell and B cell activities through different mechanisms involving activation or inhibition of IL2 production, or alteration of cells surface antigens.
Matheson et al. (1994)B-cell growth factorB-cellA quantitative but not absolute defect in B-cell growth factor production was demonstrable in one boy with hypogammaglobulinemia.
Vasto et al. (2007)interleukin-2B cellThe term "Immunological Risk Profile" (IRP), took into consideration elements like an inverted CD4:8 ratio, poor T cell proliferative responses to mitogens, low interleukin-2 production, increased numbers of CD8-positive CD28-negative cells, decreased B cell count, and later, CMV seropositivity, which also seems to play an important role in determining the IRP (Table 2) [6,7].
Rodosskaia and Chernousova (2010)interleukin-2B lymphocytesThe arising "overload" of free sulfhydryl groups inactivates antibodies of the IgM class of any specificity restoring disulphide intramolecular bonds and then the number of immune antibody-producing cells, mitotic activity of T- and B-lymphocytes and interleukin-2 synthesis are lowered and the mobility of surface immunoglobulin B lymphocytes receptors is damaged.
Murphy et al. (1987)IL-2B lymphocytesB lymphocytes from patients tested showed a direct response to recombinant interleukin (rIL-2) during culture in vitro as shown by: (a) a ligand-mediated upregulation in the level of IL-2 receptor (IL-2R) expression (12 of 12 patients), (b) an increase in cell size (eight of nine patients), (c) an increase in 3H-thymidine uptake (four of six patients).
Isacson et al. (1992)IL-2B cellsNone of the following parameters, tested prior to initiation of the therapy and 1-2 days after termination of each course of IL-2, correlated with the clinical response: WBC counts (total and differential), levels of blood CD4 and CD8 T cells, NK cells, monocytes and B cells, production of IL-1 and IL-1 inhibitor by monocytes, responsiveness to 3 mitogens, NK/LAK cell activity, and serum levels of IL-1 alpha, IL-2, soluble IL-2 receptor, and TNF alpha.
Tseng et al. (1988)IL-2B cellsAll of these results suggest that the B6.4 Ag is an early activation Ag of B cells and is functionally related to a receptor of BCGF, but not IL-2.
Adler (1989)interleukin-2B-cellsAltered function of both T- and B-cells can be shown by losses in proliferative ability and interleukin-2 and interferon synthesis.
Kehrl et al. (1986)IL 2B cellThe addition of picogram quantities of TGF-beta to B cell cultures suppressed factor-dependent, interleukin 2 (IL 2) B cell proliferation and markedly suppressed factor-dependent (IL 2 or B cell differentiation factor) B cell Ig secretion.
Saiki et al. (1984)interleukin 2B cellDissociation in the production of B cell-stimulating factors (BCGF and BCDF) and interleukin 2 by T cells from a common variable immunodeficient patient.
Furst (1995)IL-2B-cellCyclosporin A (CSA) Cyclosporin inhibits IL-2 release and T-cell activation and, secondarily, affects B-cell function.
Codias et al. (1990)IL-2B cellsSimilar to its ability to enhance anti-Ly-6A/E-induced activation of T and B cells, IFN-gamma enhanced the D7-induced inhibition of IL-2 production by alloantigen-activated normal T cells.
Bruserud (1998)IL-2B cellDecreased levels of IL-2, IL-13 and IFNgamma were observed when acute myelogenous leukaemia (AML) blasts were used instead of cells from the B cell line as accessory cells during phytohaemagglutinin activation, but the differences in IL-13 and IFNgamma levels were reversed by addition of exogenous IL-2.
Tenbrock et al. (2007)IL-2B cellsWhile some of these abnormalities explain the enhanced ability of T cells to help B cells to produce autoantibodies, decreased IL-2 production results in enhanced susceptibility to infections, reduced activation-induced cell death and prolonged survival of autoreactive T cells, which promote help to autoreactive B cells.
Coussons-Read et al. (1994)interleukin-2B lymphocytesThese conditioned alterations of immune status include a decreased in natural killer cell activity, decreased production of interleukin-2 and gamma-interferon by concanavalin A (ConA)-stimulated splenocytes and a profound suppression of the mitogenic responsiveness of T and B lymphocytes to mitogens.
Goldman et al. (1991)IL-2B cellsThese models share several features, such as productions of anti-nuclear antibodies, immune glomerulonephritis, MHC class II hyperexpression on B cells, hyper-IgE, increased IL-4 activity and impairment of IL-2 production.
Schlüter et al. (1991)IL-2B-cellThe spontaneous and cytokine (IL-4, IL-2)-induced expression of CD23 which represents a B-cell activation marker was significantly reduced during the second to fifth week postburn when compared to healthy donors.
Cohen and Yoshida (1977)lymphokineB cellsThus suppressor T cells can interfere with lymphokine production by B cells and this effect is mediated at least in part by a soluble factor.
Crispin et al. (2003)IL-2B cellsPatients with short remission periods (up to 15 years) exhibited an increased percentage of B cells; production of IL-2, IL-10 and IL-12 was decreased; production of IL-18 was increased.
Chew and Lam (2007)interleukin-2B cellsWe further show that LPXN suppressed the secretion of interleukin-2 by BCR-activated A20 B cells and that this inhibition was abrogated in the Y72F LPXN mutant, indicating that the phosphorylation of Tyr(72) is critical for the biological function of LPXN.
Edan et al. (2004)IL-2B-cellRelevant immunomodulatory mechanisms act both on T- and B-cell function, and mitoxantrone has selective immune effects in MS by decreasing levels of TNF-alpha, IL-2, IL-2R-beta1, IL-10 and IFN-gamma.