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

Full-text article links are indicated by after the article reference.

Document Target Regulator Anatomy Sentence
Chouaib and Fradelizi (1982)IL2T lymphocytesWe have observed that a complete depletion of adherent monocytes abrogates IL2 production by T lymphocytes.
Chouaib and Fradelizi (1982)IL2T cellThese results suggest that activation of a radiosensitive T cell by monokines is required for the inhibition of IL2 production.
Bettens et al. (1984)interleukin 2T lymphocytesLymphokine regulation of human lymphocyte proliferation: formation of resting G0 cells by removal of interleukin 2 in cultures of proliferating T lymphocytes.
Katsiari and Tsokos (2006)IL-2T cellsT cells from patients with SLE produce decreased amounts of interleukin-2 (IL-2), a central cytokine in the regulation of the immune response.
Katsiari and Tsokos (2006)IL-2T cellsWe discuss herein the abnormalities underlying IL-2 deficiency in SLE T cells.
Williams et al. (1996)IL-2T cellDGLA suppresses T cell activation and production of interleukin-2 (IL-2).
Bonnard et al. (1979)TCGFT cellThis loss of TCGF activity also occurred quite rapidly and was detectable within 1 hr of incubation of 0.3 ml supernatant with 2 to 5 x 10(7) CTC at 23 degrees C. 2 x 10(8) mononuclear peripheral blood leukocytes were not effective in removing TCGF activity, and incubation with similar numbers of cells from B and T cell lines had no effect.
Landsverk et al. (2002)IL-2 geneT-cellThe normally repressed IL-2 gene is transcribed in nuclei from quiescent human T cells and from various non-T-cell lines.
Pahlavani and Richardson (1996)IL-2T cellsThe age-related decline in IL-2 production has been shown to arise from a decline in IL-2 transcription, and a recent study suggests that the transcription factor NFAT (nuclear factor of activated T cells) may play a role in the decline in IL-2 transcription.
Arya et al. (1984)cell growth factorT cellDexamethasone-mediated inhibition of human T cell growth factor and gamma-interferon messenger RNA.
Domingo et al. (1985)interleukin-2T lymphocytesT8-depleted and unfractionated T lymphocytes allogeneically stimulated and cultured in the presence of pregnancy sera exhibit an inhibition of cellular proliferation and interleukin-2 synthesis, respectively.
Sasagawa et al. (2006)interleukin-2T cellsEchinacea alkylamides inhibit interleukin-2 production by Jurkat T cells.
Pinkston et al. (1987)interleukin 2T lymphocytesCorticosteroid therapy suppresses spontaneous interleukin 2 release and spontaneous proliferation of lung T lymphocytes of patients with active pulmonary sarcoidosis.
Pinkston et al. (1987)IL 2T cellIn contrast, over the same period, the treated group had marked reduction of spontaneous lung T cell release of IL 2 and proliferation (p less than 0.01, all comparisons before therapy).
Pinkston et al. (1987)IL 2 geneT lymphocytesThese observations are consistent with the concept that directly, or indirectly, corticosteroids are capable of suppressing the IL 2 gene in activated T lymphocytes in vivo.
Dautry-Varsat et al. (1988)IL-2T-cellCsA also prevents the constitutive secretion of IL-2 in this T-cell line by blocking transcription of the IL-2 gene.
Dautry-Varsat et al. (1988)IL-2T cellsWe also show for the first time, that CsA not only can inhibit IL-2 production of T cells upon activation, but that it can also prevent ongoing constitutive IL-2 synthesis of a T-cell line.
Cech et al. (2006)IL-2T cellsEchinacea alkylamides suppressed IL-2 secretion by stimulated T cells, and this effect was significantly lessened upon oxidation of the alkylamides to carboxylic acids and hydroxylated metabolites.
Claudette et al. (1990)interleukin 2T cellMechanism of phosphatidylserine-induced inhibition of interleukin 2 synthesis in the human T cell line Jurkat.
Claudette et al. (1990)Interleukin-2T cellsTreatment of Jurkat T cells with PS, results in a strong decrease of Interleukin-2 synthesis.
Manger et al. (1986)IL-2T cellAnother T cell line, HUT 78, also produces IL-2 in response to a rise in [Ca++]i and PMA; however, in HUT 78, PMA alone induces low levels of IL-2 production that is not blocked by CsA.
Manger et al. (1986)IL-2T cellThese data suggest that CsA does not globally inhibit IL-2 gene expression, but rather interferes with signaling events of T cell activation.
Ponner et al. (1998)IL-2T-cellFollowing interleukin-2 (IL-2) deprivation, phytohaemagglutinin (PHA)/IL-2 expanded human T-cell lines were irradiated with UV-B light to induce apoptosis, confirmed by propidium iodide staining of Triton X-100-lysed cells.
Kabelitz and Al-Gorany (1989)IL-2T cellEsculetin inhibits T cell activation without suppressing IL-2 production or IL-2 receptor expression.
Kabelitz and Al-Gorany (1989)IL-2T cellsEsculetin did not inhibit interleukin-2 (IL-2) production, nor did it interfere with the appearance of IL-2 receptors on stimulated T cells, as judged by immunofluorescence using anti-Tac monoclonal antibody.
Beaurain et al. (1989)IL-2T cellsMoreover, a significantly decreased IL-2 activity was detected in the supernatants of stimulated T cells from hemodialyzed patients (mean +/- SEM: 0.93 +/- 0.12 U/ml in patients vs. 2.49 +/- 0.22 U/ml in normal controls, P less than 0.0001).
Freedman et al. (1992)IL-2T cellsChTX inhibited proliferation of PBMC and purified T cells, decreased IL-2 elaboration 15 h after stimulation by 78.4 +/- 5.3% (n = 5), and decreased IL-2 mRNA steady-state levels by 80% between 8 and 10 h after stimulation.
Carding and Reem (1987)interleukin-2T cellDexamethasone and Cyclosporin A (CsA) which inhibit early events of T cell activation and the expression of the interleukin-2 (IL-2) and gamma-interferon (gamma-IFN) genes also markedly suppress the expression of c-myc mRNA in Con A, and Con A + TPA-activated thymocytes.
Hess et al. (1982)TCGFT lymphocyteThis inhibition was found to be associated with the inhibition of T lymphocyte stimulating growth factor(s) (TCGF) production in the supernatants of secondary MLR cultures.
Chen (2001)interleukin-2T cellTriptolide inhibits both Ca(2+)-dependent and Ca(2+)-independent pathways and affects T cell activation through inhibition of interleukin-2 transcription at a site different from the target of cyclosporin A.
Shephard and Shek (1995)interleukin-2T cellThe production of interleukin-2 is decreased, sometimes with a decrease of total T cell count, and often with changes in T cell subsets and proliferative responses to mitogens.
Hooks (1994)interleukin 2T-lymphocyteThe mechanism of action is similar to that of cyclosporine in that it ultimately blocks the production of interleukin 2, thereby inhibiting further T-lymphocyte proliferation.
Tsoukas et al. (1984)interleukin-2T lymphocytesThe hormonal form of vitamin D3, 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], at picomolar concentrations, inhibited the growth-promoting lymphokine interleukin-2, which is produced by human T lymphocytes activated in vitro by the mitogen phytohemagglutinin.
Goebels et al. (1988)IL-2T cellThe data indicate the possibility of paracrine growth stimulation via IL-2 and its receptor even in those human T lymphotropic virus I-infected T cell populations that apparently lack IL-2 activity when analyzed by conventional assay procedures.
Wacholtz et al. (1991)IL2T cellsOther cyclic adenosine monophosphate (cAMP) elevating agents (forskolin, isoproterenol, and the cAMP analogue, dibutyryl cAMP) also inhibited lectin-stimulated IL2 production by T cells, but could not inhibit IL2 production by Jurkat cells.
Morikawa et al. (1994)IL-2T cellsAt concentrations of 1.6 to 40 micrograms/ml, these drugs suppressed interleukin-2 (IL-2) production induced by mitogen-stimulated T cells, but not the expression of IL-2 receptor (CD25), in a dose-dependent manner.
Morikawa et al. (1994)IL-2T cellsTherefore, the suppressive action on T-lymphocyte proliferation seems to be based on the ability of these drugs to inhibit IL-2 production by T cells.
Yang et al. (1994)interleukin-2T-lymphocyteTriptolide suppresses T-lymphocyte proliferation by inhibiting interleukin-2 receptor expression, but spares interleukin-2 production and mRNA expression.
Paul and Baumann (1989)interleukin-2T-lymphocytesImpaired interleukin-2 production by T-lymphocytes in polycythemia vera.
Webster (2000)interleukin-2T-cellReductions in B- and T-cell immunity and in levels of interleukin-2 are age related.
Ramarli et al. (1987)IL-2T lymphocytesPerhaps more importantly, T3-Ti-mediated IL-2 inhibition of this type is not operational in peripheral T lymphocytes.
Ramarli et al. (1986)IL-2T lymphocytesPerhaps more importantly, T3-Ti-mediated IL-2 inhibition of this type is not operational in peripheral T lymphocytes.
Tsoi et al. (1984)IL-2T cellsWe analyzed various cellular functions in the pathway of T cell activation and found that in patients with immunodeficiency, (1) their M phi usually could process and present antigens to normal T cells, (2) their T cells did not proliferate even in the presence of normal antigen-pulsed M phi, (3) IL-2 production by T cells was deficient, and (4) exogenous IL-2 restored CML activity in cells of most patients early after grafting but not in cells of most patients with chronic GVHD.
Tsoi et al. (1984)IL-2T cellTherefore, failure to induce proliferation and cytotoxicity in T cells of marrow recipients is not likely due to M phi defects but because of ineffective communication among T cell subsets, probably related to impaired IL-2 production and/or unresponsiveness to IL-2.
DiSanto et al. (1990)interleukin 2T cellsAbsence of interleukin 2 production in a severe combined immunodeficiency disease syndrome with T cells.
DiSanto et al. (1990)IL-2T cellThis patient's immunological defect appears to be attributable to a selective deficiency in T cell production of IL-2, which may reflect a subtle abnormality in the IL-2 gene locus or a defect in a regulatory factor necessary for IL-2 transcription.
Chen et al. (1986)IL2T cellsIn contrast to the impairment of IL2 production, the amount of IFN gamma secretion by elder human T cells was almost at the same level as that by young human T cells.
Dohlsten et al. (1987)interleukin-2T cellsHistamine acts directly on human T cells to inhibit interleukin-2 and interferon-gamma production.
Dohlsten et al. (1987)IL-2T-cellThe conclusion that histamine acts directly on T cells and does not require accessory cells to induce suppression is further confirmed by the demonstration that IL-2 production by the human T-cell leukemia line Jurkat was significantly suppressed by histamine in a H-2 receptor-restricted manner.
Klingemann et al. (1986)IL2T lymphocyteThus it is very likely that PGE2 inhibits T lymphocyte proliferation, not exclusively by inhibition of IL2 production or activity.
Rabinowich et al. (1985)IL-2T cellsThis would indicate that the reduced cellular responsiveness in aging may be related both to a defect of IL-2 receptor expression on T cells of aged subjects and to an impairment in the endogenous IL-2 synthesis in the aged individuals.
Rezai et al. (1990)IL-2T cellInhibition occurred during the inductive phase of the cell cycle, since histamine added 24 hours after PHA-P stimulation had no effect on subsequent T cell proliferation, and was attributable to inhibition of interleukin-2 (IL-2) gene expression.
Rezai et al. (1990)IL-2T cellsThese findings indicate that histamine exerts its anti-proliferative effects on T cells by inhibiting IL-2 production, via blockade of IL-2 gene expression.
Ghezzi et al. (1997)interleukin-2T lymphocytesIn addition to the progressive loss of CD4 "helper" T lymphocytes, a profound defect in interleukin-2 (IL-2) production was recognized as a major pathogenic component of the new disease.
Hopkins and Failla (1999)IL-2T lymphocyteCopper deficiency reduces secretion of the cytokine interleukin-2 (IL-2) by activated rodent splenocytes, human peripheral blood mononuclear cells and Jurkat cells, a human T lymphocyte cell line.
Hopkins and Failla (1999)IL-2 geneT lymphocytesThese data indicate that decreased cellular Cu attenuates IL-2 synthesis in T lymphocytes by inhibiting transcription of the IL-2 gene.
Bennett et al. (1990)IL-2T-cellThese results indicate that extracts from hydatidiform mole trophoblast contain immunosuppressive factors that block human T-cell clonal expansion by inhibiting the utilization and/or production of IL-2.
Randak et al. (1990)IL-2T lymphocytesThese observations support the conclusion that the suppression of factor binding to the Pu-boxes by CsA impairs the activity of IL-2 and of further lymphokine genes, thereby inhibiting the synthesis of lymphokines in T lymphocytes.
Krönke et al. (1984)TCGFT-cellSpecifically, inhibition of T-cell growth factor (TCGF; also designated interleukin 2) production appears to be an important pathway by which CsA impairs T-cell function.
Sutton et al. (2004)interleukin-2T cellsHuman immunodeficiency virus type 1 (HIV-1) infection decreases the production of interleukin-2 (IL-2) from CD4+ and CD8+ T cells.
Childerstone et al. (1989)IL2T cellsBoth IL2 and IL2 receptors were diminished and delayed when T cells were stimulated with SP as compared with TT.
Gmünder et al. (1990)IL-2T cellsThe addition of relatively high concentrations of GSH (5 mM) to cultures of concanavalin A (Con A)-stimulated splenic T cells was found to augment strongly the DNA synthesis but inhibited the production of IL-2.
Baumann et al. (1991)IL-2T-cellThe structurally unrelated immunosuppressive drugs cyclosporin A (Sandimmun) and FK-506 both interfere with the process of T-cell proliferation by blocking the transcription of the T-cell growth factor interleukin-2 (IL-2).
Nath et al. (1984)IL-2T cellMoF from borderline and lepromatous patients produced 52-61% inhibition of human interleukin-2 (IL-2) production by a PHA conditioned T cell line (Jurkat).
Nath et al. (1984)IL-2T cellsIt is possible that the unresponsiveness associated with lepromatous leprosy is related to the inhibition of IL-2 production by suppressive factors, thereby, preventing the further expansion of antigen reactive T cells.
Reeves et al. (1985)TCGFT cellUtilizing dexamethasone (DEX), a known inhibitor of TCGF production, reductions in T cell proliferation, TCGF production, and TCGF receptor expression, as measured by TCGF adsorption and Tac acquisition, were demonstrated after PHA stimulation.
Meuer et al. (1989)interleukin-2T-cellThis defect prevents production of interleukin-2 during T-cell activation after antigen contact.
Dornand et al. (1986)IL 2T cellOn the other hand, we observed that: ouabain inhibited the expression of the receptors for IL 2, an obligatory step in lymphocyte proliferation; ouabain blocked the proliferation of an IL 2 sensitive human T cell line; in both cases the inhibition paralleled that of lymphocyte proliferation.
Creemers et al. (1986)IL-2T cellsWe conclude that a defect in IL-2 production is associated with human T-cell lymphotropic virus III infection, but that the expression of the IL-2 receptor on T cells is not greatly affected.
Hopkins and Failla (1997)IL-2 mRNAT-lymphocytesCopper deficiency reduces interleukin-2 (IL-2) production and IL-2 mRNA in human T-lymphocytes.
Pawelec et al. (2004)cell growth factor interleukin-2T cellsUsing T cells from young donors to model the process of T cell clonal expansion in vitro under these conditions reveals age-associated increasing levels of oxidative DNA damage and microsatellite instability (MSI), coupled with decreasing DNA repair capacity, telomerase induction and telomere length, decreased levels of expression of the T cell costimulator CD28 and consequently reduced secretion of the T cell growth factor interleukin-2 (IL-2).
Aussel et al. (1993)interleukin-2T cellIn contrast, choline transport-inhibitors such as hemicholinium-3, decamethonium and dodecyltrimethylammonium do not inhibit interleukin-2 synthesis and proliferation of the Jurkat T cell line.
Aussel et al. (1993)interleukin-2T cellThe inhibition of interleukin-2 synthesis appeared to be mediated through the inhibition of diacylglycerol production induced by T cell activators.
Aussel et al. (1993)interleukin-2T cellA major role for phosphatidylserine in the regulation of T cell activation emerged, since we demonstrated that a panel of K+ channel blockers enhanced the synthesis of this phospholipid mimicking the previously described effect of exogenously added phosphatidylserine in Jurkat cells, i.e., a blockade of interleukin-2 synthesis probably due to a defect in diacylglycerol production.
Averill et al. (1988)IL-2T-cellActivation of adenylate cyclase, inhibition of cAMP-dependent phosphodiesterase, or the direct addition of the cell-permeable cAMP analog, 8-N3-cAMP, increased occupancy of intracellular cAMP receptors, inhibited IL-2 production, and reduced T-cell proliferation.
Moss et al. (1984)TCGFT cellsHowever, hydrocortisone was able to inhibit TCGF production by cloned T cells.
Matsuzaki et al. (1989)IL-2T cellIt failed to inhibit CD 25 expression and IL-2 production by T cell blasts in the T cell activation phase, but completely blocked recombinant IL-2-induced proliferation of T cell blasts in the T cell proliferation phase.
Booth et al. (1984)IL-2T cellSelective removal of IL-2 from crude or partially purified IL-2 preparations by extensive adsorption with activated murine thymocytes or an IL-2-dependent T cell line completely eliminated SE-PFC-inducing activity, indicating that IL-2 itself was necessary for the effect.
Lea et al. (1989)IL-2T lymphocytesThus, both IL-2 production and IL-2 receptor expression of activated T lymphocytes are severely impaired.
Rigby et al. (1987)IL-2T cellThe steroid hormone, 1 alpha,25-dihydroxyvitamin D3 (calcitriol), has been shown to inhibit T cell proliferation, primarily through inhibition of interleukin 2 (IL-2) production.
Isgrò et al. (2002)IL-2T cellCompared with uninfected controls, an altered cytokine and chemokine production by BM cells was observed before treatment, characterized by decreased interleukin 2 (IL-2) and elevated tumour necrosis factor-alpha, macrophage inflammatory protein (MIP)-1alpha, MIP-1beta, and RANTES (regulated on activation, normal T cell-expressed and secreted) levels, along with a defective BM clonogenic activity.
Chandy et al. (1984)IL-2T lymphocyteThe expression of the IL-2 receptor (Tac) during T lymphocyte activation was not altered by K channel blockers, whereas the production of interleukin 2 (IL-2) was reduced to the level in unstimulated T lymphocytes.
Krönke et al. (1985)IL-2T cellsHowever, mitogenic stimuli activate IL-2 receptor gene expression in normal T cells, whereas these stimuli paradoxically inhibit IL-2 receptor gene transcription in HTLV-I-infected leukemic T cells.
Huleatt et al. (2003)IL-2T cellsT cells deficient in p27kip1 expression showed an impaired ability to undergo cell cycle arrest in response to IL-2 deprivation.
Frankel and Kerdel (2001)IL-2T-cellTacrolimus, available for intravenous, oral and now topical administration, is a potent immunosuppressive agent with the ability to block the production of Interleukin-2 (IL-2) and inhibit T-cell proliferation.
Dijkmans et al. (1996)IL-2T cellsThis synergy is probably based on different mechanisms of action of the 2 drugs: CsA primarily inhibits the production of interleukin 2 (IL-2) (and other cytokines) at the level of transcription, whereas chloroquine primarily inhibits the responsiveness of T cells to IL-2 stimulation.
Hinoshita et al. (1990)IL-2T cellsThe IL-2 production of T cells, when stimulated with autologous non-T cells separated on a polystyrene resin column, was significantly decreased in patients with minimal-change nephrotic syndrome.