Viewing negative 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
Gillies et al. (1992)IL2T-cellThe fusion of IL2 to the carboxyl terminus of the immunoglobulin heavy chain did not reduce IL2 activity as measured in a standard proliferation assay using either mouse or human T-cell lines.
Kusugami et al. (1991)interleukin-2T cellsMucosal CD8+ T cells and plastic-adherent cells were unable to suppress interleukin-2 activity by autologous or allogeneic CD4+ T cells.
Kusugami et al. (1991)interleukin-2T cellsFinally, supernatants from Crohn's disease and ulcerative colitis cell cultures failed to suppress interleukin-2 production by control CD4+ T cells.
Gmünder et al. (1990)IL-2T cellModerate intracellular GSH levels, however, are apparently not inhibitory for IL-2 production, since intracellular GSH depletion by cysteine starvation or by graded concentrations of DL-buthionine sulfoximine (BSO) had virtually no effect on IL-2-specific mRNA expression and the production of T cell growth factor (TCGF).
June et al. (1989)IL-2 geneT-cellIn contrast, IL-2 gene expression and T-cell proliferation induced by CD28 MoAb plus PMA were unaffected by cyclosporine.
Miyawaki et al. (1982)TCGFT cellsIn contrast, absorption of TCGF by PHA-induced blasts was not significantly reduced even when they were pretreated with other monoclonal antibodies (anti-Ia, OKT9, or OKT10) with specificity for antigens expressed on activated T cells.
Katzen et al. (1985)IL 2T cellsThe failure of IL 2 secretion was not caused by down-regulation of IL 2 production by IL 2 itself, because the addition of IL 2 to cultures of T cells stimulated with PHA in the presence of monocytes did not interfere with IL 2 production.
Noma et al. (1989)IL-2T cellsOvalbumin (OVA)-induced IL-2 responsiveness of lymphocytes from patients with hen-egg allergy was not suppressed by the supernatant from Df-stimulated T cells, indicating the antigenic specificity of the effect.
Santoli et al. (1990)IL-2T cellDihomogamma linoleic acid (DGLA), AA, and their metabolites (PGE1 and PGE2, respectively) strongly inhibited short- and long-term growth of IL-2-dependent T cell cultures; EPA was much less inhibitory and its product, PGE3, failed to suppress IL-2 responses.
Parhar et al. (1989)IL-2T lymphocyteWe have earlier shown that first trimester human decidual cells and decidual macrophages suppress T lymphocyte alloreactivity in an MHC-unrestricted manner by secreting PGE2, which blocks the generation of IL-2 receptors (IL-2R) and production of IL-2 by lymphocytes but does not interfere with the interaction between IL-2 and IL-2R or the lytic function of CTL, once generated.
Laurent et al. (1986)IL2T cellsThese findings showed that IL2 receptor expression is not restricted to activated T cells, and raise the question of the possible role of IL2 in the regulation of malignant B cell clone expansion.
Szamel et al. (1995)IL-2T-cellIn human peripheral blood lymphocytes stimulated via the T-cell antigen receptor/CD3 complex IL-2 synthesis and cellular proliferation were effectively inhibited by a concentration of ouabain as low as 50 nM, whilst the expression of high affinity IL-2 receptors was not influenced.
Hayward et al. (1988)IL-2T cellsProliferative responses by T cells from newborn cord blood stimulated with PHA or CD3 were reduced following infection with live (but not killed) herpes simplex virus in vitro although activation (measured by calcium flux) and IL-2 production were unaffected.
Marazuela et al. (1995)IL-2T cellsThese abnormalities were not associated with a defective IL-2 production by T cells, nor with a decreased IL-2R expression.
Yanagi et al. (1992)interleukin 2T cellNorthern blot analysis indicated that the expression of genes induced during T cell activation, such as those encoding interleukin 2 (IL-2), c-myc, IL-2 receptor, IL-6, c-myb, and cdc-2, was not significantly suppressed in MV-infected cells, suggesting that MV does not interfere with the T cell activation process.
Secrist et al. (1994)IL-2T cellsThis effect was tissue specific and IL specific in that 1) primed peripheral blood T cells had only one peak of IL-4 mRNA expression at 8 h and 2) in primed tonsillar T cells, mRNA expression of IL-2, IL-6 and IL-2 receptor and c-myc was not delayed.
Gertsch et al. (2003)Interleukin-2T cellsInterleukin-2 (IL-2), and-6 (IL-6) mRNAs levels were not influenced markedly by curcumin in stimulated PBMCs, but significantly reduced in stimulated Jurkat T cells.
Björk et al. (1997)IL-2T cellsThe prevalence of IL-2-, IFN-gamma-, and TNF-beta-producing T cells was not reduced by CNI-1493.
Mahaffey and Mummert (2007)IL-2T cellSurprisingly, an anti-CD44 Ab antagonistic for HA binding did not reduce IL-2 secretion or T cell proliferation.
Mouzaki et al. (1992)IL-2T cellsHowever, if T cells are activated in the presence of either drug, their proteins not only fail to derepress, but efficiently and irreversibly silence IL-2 transcription.
Becher et al. (1999)IL-2T cellsFurthermore, the capacity of T cells to secrete IFN-gamma upon restimulation when previously treated with TNFR:Fc is impaired, whereas IL-2 secretion was not altered.
Tohma et al. (1991)IL-2T cellsMoreover, DNA synthesis and IL-2 production by immobilized anti-CD3-stimulated CD4+ T cells were not suppressed by the mAb to LFA-1 or ICAM-1.
Brown et al. (1988)IL-2T cellsThis response of T cells to IL-4 plus PMA is independent of the action of IL-2 as judged by 1) the lack of IL-2 in supernatants of stimulated cells, 2) the failure to detect IL-2 mRNA in stimulated cells by in situ hybridization, 3) the inability of anti-IL-2R antibody and of anti-IL-2 antibody to block responses to IL-4 plus PMA, and 4) the failure of cyclosporin A to block responses.
Henrickson et al. (1995)IL-2T cellsBoth prolonged skin allograft survival, preferentially depleted CD4+ T cells, downregulated IL-2 secretion, and failed to inhibit CTL.
Okino et al. (1993)Interleukin-2AS-9Interleukin-2, IL-2R alpha, and beta messages are not down-regulated by the AS-9 SF and the suppressive effect of the AS-9 SF on IL-2R alpha expression and on T cell proliferation is not neutralized by the addition of exogenous recombinant IL-2.
Kennedy et al. (1997)IL-2T cellOral administration of PLP139-151 did not reduce IL-2 or IFN-gamma production and appeared to increase Ag-specific T cell proliferation.
Tanaka et al. (1995)IL-2T cellConcerning T cell surface molecule gene expression in our modified MLC, IL-2 receptor gene expression was not altered so much in allo BMT patients, however, CD28 and CTLA-4 gene expression were elevated in patients with graft failure and severe acute GVHD.
Sung et al. (2003)IL-2T cellThese data show that CD28's modulation of T cell responses to TGF-beta1 is not via the production of high levels of IL-2, and suggest that engagement of CD28 may activate additional downstream pathways that modulate the responses of naïve T cells to TGF-beta1.
Langston et al. (2003)IL-2T cellHere we report that E-NTPDase activity is up-regulated within 15 min of T cell stimulation and that reversible and irreversible enzyme inhibitors profoundly reduce secretion of IL-2 and IFN-gamma, but not IL-4.
Saito et al. (2008)IL-2T cellsCONCLUSION: In the patient who does not develop CSS even after repeat EP, the frequency of Tr1 and the ability of responder T cells to generate IL-2 do not decrease, but show a remarkable decrease in the EP patient who develops CSS.
Hashimoto et al. (2005)IL-2T cellThe amount of IL-17 produced by T cell clones stimulated with immobilized anti-CD3 Ab plus soluble anti-CD28 Ab was negatively, but only weakly, correlated with that of IL-4, but not correlated with IL-2, IL-5, IL-13, and IFN-gamma production.
Yang et al. (1997)IL-2T cellThe transcripts of interleukin-10 (IL-10) and interferon-gamma (IFN-gamma) genes of these two T cell lines were evidently increased in the presence of SLE sera, while IL-2 and IL-4 were unaffected.
Nori et al. (2003)IL-2T cellRESULTS: Ebastine inhibited T cell proliferation and the production of IL-4, IL-5, IL-6, and TNF-alpha by T cells under each co-stimulatory condition tested, whereas it exhibited no effect on the production of IL-2 or IFN-gamma.
Jin et al. (2003)interleukin 2T cellsFurther, S1P or DHS1P but not ceramide or sphingosine enhanced rather than decreased secretion of interleukin 2 and interferon gamma by T cells stimulated with anti-CD3 plus anti-CD28.