Viewing negative mentions of positive regulation of Il2 (M. musculus) in T cells

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Pucci et al. (1998)IL-2 mRNAT cellsWe found that the IL-2 mRNA level in T cells from young but not from old mice increased up to 6- to 10-fold by addition of cycloheximide (CHX) while the stability of IL-2 mRNA is not affected.
Novak and Rothenberg (1990)interleukin 2T cellscAMP inhibits induction of interleukin 2 but not of interleukin 4 in T cells.
McCoy et al. (1985)IL 2T cellsHowever, in vivo administration of Con A to old NZB mice did not induce the expression of IL 2 receptors on Lyt-2+ T cells.
Liang et al. (1998)IL-2T cellsFirst, the poor IL-2 production in lpr DN cells could not be restored by supplement of signals known to augment IL-2 response in normal T cells.
Liang et al. (1995)IL-2T cellsThey also increased significantly IL-2 and IL-2R alpha gene expression in T cells of burn mice, but not up to the normal control.
Itoh et al. (1988)interleukin-2T-cellMonocyte-independent interleukin-2 production and proliferation of human T cells in response to murine hybridomas expressing the OKT3 monoclonal antibody: interleukin-1 is not required for T-cell proliferation.
Soong and Tarleton (1994)IL-2 mRNAT cellsOur previous observation that reduction of IL-2 mRNA in T cells from T. cruzi-infected mice is not due to an increased degradation of the mRNA suggests a repression of the IL-2 gene at the transcriptional level.
Telander et al. (1999)IL-2T cellsHeterokaryons formed by the fusion of anergic murine T cells to normal murine T cells also failed to accumulate intracellular IL-2 protein in response to stimulation either with the combination of CD3 and CD28 mAbs or with ionomycin plus a protein kinase C-activating phorbol ester.
Berebbi et al. (1983)TCGFT-cellA differentiated T-cell function (i.e., cytolysis) persists and the differentiated line does not require TCGF.
Nagarkatti et al. (1994)IL-2T-lymphocyteIn the current study we describe the spontaneous in vitro transformation of T-lymphocyte cell lines during routine cell culture as evidenced by autonomous growth without any requirement for stimulation or exogenous interleukin 2 (IL-2).
Röllinghoff et al. (1983)IL-2T cellsThe following results were obtained: activated T cells, triggered by cell antigen or Con A as well as cells of a CTL-clone, but neither LPS-activated B cells nor tumour cells absorbed IL-2; IL-2 was absorbed in a doses dependent fashion until saturation of the absorbing cells; IL-2 absorption occurred within minutes and was temperature-dependent; data comparing activated T cells versus gluteraldehyde-treated activated T cells in repeating absorptions suggested that with gluteraldehyde-treated cells only absorption of IL-2 by the exposed IL-2 receptors is measured, while metabolically active cells seem to assay, besides of the mere binding of IL-2, also an enzymatic event, which probably follows binding of IL-2 to its receptor.
Chang et al. (1992)IL2T-cellMechanism of immunosuppressive effect of alprazolam: alprazolam suppresses T-cell proliferation by selectively inhibiting the production of IL2 but not acquisition of IL2 receptor.
Tarleton (1988)IL-2T cellsAlthough Con A can provide either of the signals necessary for IL-2 production, calcium flux or protein kinase C activation, to T cells from normal mice, Con A in combination with either calcium ionophore or phorbol ester failed to activate T cells from infected mice to produce IL-2.
Kupper et al. (1987)interleukin 2T cellsAutocrine growth of T cells independent of interleukin 2: identification of interleukin 4 (IL 4, BSF-1) as an autocrine growth factor for a cloned antigen-specific helper T cell.
Soong and Tarleton (1992)IL-2 mRNAT cellsThese data suggest that the reduction of IL-2 mRNA in infected mice is not the result of an increased degradation of its mRNA but to down-regulation of transcription of the IL-2 gene in T cells from T. cruzi-infected mice.
Ofosu-Appiah et al. (1996)IL-2T cellWhen cultured with either heparan sulfate or Concanavalin A, the T cell clones produced high levels of IL-4 and IL-5 with no detectable IL-2 or IFN-gamma.
Wagner and Heeg (1988)IL-2T cellsWe show that CR cross-linking of resting murine CD8+ T cells seeded at low cell densities is insufficient to induce responsiveness to the growth-promoting effect of interleukin-2 (IL-2), i.e. fails to induce expression of functional IL-2 receptors.
Hengel et al. (1991)IL2T cellDissection of signals controlling T cell function and activation: H7, an inhibitor of protein kinase C, blocks induction of primary T cell proliferation by suppressing interleukin (IL)2 receptor expression without affecting IL2 production.
Lai et al. (2009)IL-2T-cellThe results showed neutralization of murine IL-2 did not ablate the effect of rhIL-2 on CD8+ T-cell viability at 72 hours after stimulation (Figures 3B), demonstrating that the function of exogenous IL-2 is not to induce more murine IL-2 production.
Zuckerman et al. (1998)IL-2T cellIn Th1 clones, activation by ProAd-ICAM induces very transient IL-2 mRNA expression that does not result in detectable IL-2 secretion or T cell proliferation.
Tarleton (1988)IL-2T cellsThese results suggest that the inability of T cells from T. cruzi-infected mice to produce IL-2 in vitro in response to Con A is not due to the lack of IL-2-producing cells, but may be the result of the maturational state of the T cells or to the presence of a suppressor population.
Reyes et al. (1986)IL-2-inducedT cellsThus, neither T cells nor NK cells are required for IL-2-induced IFN-alpha/beta production by BM cells.
Hammond et al. (1993)interleukin 2T cellThese cells fail to acquire interleukin 2 (IL-2) receptors, produce IL-2, and proliferate when activated with mitogens or monoclonal antibodies (mAbs) against the T cell receptor (TCR).
Blackman et al. (1991)IL-2T cellsIn this report, we show that the anergic CD4+ T cells did not mobilize calcium or express receptors for interleukin 2 (IL-2) following TcR ligation.
Cattan et al. (2003)IL-2T-cellThe protective effect of high-dose streptozotocin was lost in older male NOD mice. betaTC-tet cells did not stimulate autoreactive T-cell hybridomas, but induced IL-2 secretion by splenocytes from diabetic NOD mice.
Chang et al. (1988)IL-2T cellsExperiments based on mixtures of nylon wool-enriched splenic T-cell and adherent cells and on anti-MAC-1 plus complement-treated spleen cells indicated that (a) adherent cells are not required for T-cell production of IL-3, unlike IL-2 production, and (b) the decrease in IL-3 production with age is due solely to alteration in IL-3-producing T cells.
Palacios and Leu (1985)IL-2T cellsThe additive activity of IL-1 on growth of normal T cells is not due to increased production of IL-2 in the cultures or induction of normal T cells to expression of IL-2 receptors by IL-1.
Thornton et al. (2004)IL-2T cellsThese results are most compatible with a model in which CD4(+)CD25(+) T cells do not suppress the initial activation of CD4(+)CD25(-) T cells, but mediate their suppressive effects following production of IL-2 by the responder cells resulting in both the expansion of the CD4(+)CD25(+) T cells and the induction of their suppressor function.
Yang and HayGlass (1993)IL-2T cellsIn contrast to the finding that IL-2 is not required for IL-4 gene expression by primed T cells in allergen-driven responses, both induction and expression of IFN-gamma responses are strictly IL-2 dependent.
Yang and HayGlass (1993)IL-2T cellsAlthough de novo induction of IL-4 and IFN-gamma production obtained after in vitro activation of cells from naive animals with immobilized anti-CD3 is IL-2 dependent, Ag-driven IL-4 synthesis by CD4 T cells from OVA (alum)- or ragweed extract (alum)-immunized mice is independent of IL-2.
Yamashita and Boros (1990)IL-2T cellsElimination of L3T4+ T cells diminished, and the Lyt-2+ T cells left unchanged IL-2 production in the acute infection cells.
Rockwell et al. (2006)IL-2T cellsLikewise, 2-AG suppressed the transcriptional activity of two transcription factors crucial for IL-2 expression, nuclear factor of activated T cells and nuclear factor kappaB, in the absence but not in the presence of T0070907. 2-AG treatment also induced PPARgamma binding to a PPAR response element in activated Jurkat T cells.
Stanley et al. (1989)IL-2T cellWe have identified a murine pork insulin/IAd-specific T cell hybridoma, B8P3.11, in which perturbation of the B8P3.11 TCR by either Ag in association with Ia, anti-CD3 antibodies, or a mitogenic lectin does not induce increases in myo-inositol 1,4,5-triphosphate production or cytosolic free calcium, yet it does lead to IL-2 secretion.
Heckford et al. (1986)IL 2T cellStimulation of T cell clones with recombinant IL 2 resulted in proliferation and sustained expression of the c-myc cellular proto-oncogene, but did not induce the expression of mRNA for the lymphokines IFN-gamma and IL 2.
Kaplan et al. (2003)interleukin-2T cellsWith the demonstration that cannabinoid-induced inhibition of PMA/Io-stimulated interleukin-2 was not mediated via CB1 or CB2, alternative targets of cannabinoids in T cells were examined.
Tanaka et al. (1991)IL-2T cellsThe effect of IL-4 on IL-2 production was not due to prolongation of survival or to enhanced proliferation of T cells.
Lai et al. (2009)IL-2T cellSince the action of IL-2 on CD8+ T cell expansion was most effective during the first 2.5 hours after stimulation (Figure 2A), CD25 up-regulation may not be responsible for the IL-2 signal in early priming stage.
Yang and Hayglass (1993)IL-2T cellsT cells from mice immunized with allergen in complete Freund's adjuvant (CFA) generate strong IL-2 and IFN-gamma production, but virtually no IL-4, while unimmunized mice do not respond detectably to allergen in vitro (< 1 U).
Tsuchida et al. (1992)IL-2T cellThus, the intermediate TCR cell-enriched population could not respond to a T cell mitogen, Con A, but responded well to a super antigen, staphylococcal enterotoxin B, and IL-2.
Suzuki et al. (1995)IL-2 mRNAT cellsHowever, it did not increase the levels of IL-4 mRNA at all and only partially increased those of IL-2 mRNA in anergic T cells.
Kane et al. (2001)IL-2T cellsRetrovirus-mediated expression of activated Akt in primary T cells from CD28-deficient mice is capable of selectively restoring production of IL-2 and interferon gamma, but not IL-4 or IL-5.
Grammer et al. (1988)IL-2T cellsThere was no requirement for the addition of exogenous IL-2 to the culture and, since murine B cells do not appear to express either membrane or secreted IL-1, this lymphokine appears to either not be required for the activation of virus-specific CTL or to be provided by the T cells themselves.
Guo et al. (1993)IL-2T cellAnti-murine CD44 antibodies by themselves did not induce the production of IL-2 by antigen-specific T cell hybridomas.
Granstein et al. (1984)IL 2CTLHowever, these cells do provide a signal(s) other than hapten necessary for CTL activation because ABA-coupled high density spleen cells do not activate CTL cells, even with the addition of IL 2.
Duffy et al. (2006)interleukin-2T cellsUsing T cells from transgenic interleukin-2-deficient mice we showed that interleukin-2 was not required for a secondary response, although it was necessary for a primary response.
Vissinga et al. (1990)IL-2T cellFrom these data it can be concluded that the reduced DTH responses in old mice are not solely due to CD8+ suppressor cell activity and/or lack of IL-2, but that rather intrinsic defects of the CD4+ T cell population appear to play a major role in the impaired DTH reactivity during ageing.
Saoulli et al. (1998)IL-2T cellsIn support of a functional role for TRAF2 in 4-1BB signaling, we find that resting T cells isolated from TRAF2-deficient mice or from mice expressing a dominant negative form of TRAF2 fail to augment IL-2 production in response to soluble 4-1BBL.
Schmitt et al. (1994)IL-2T cellsIn addition, the use of T cells from IL-4 knockout mice elucidated that the basic (IL-2 + TGF-beta) mediated IL-9 production is independent of IL-4.
Harris et al. (2004)IL-2T cellsFull stimulation of anergic A.E7 T cells fails to enhance IL-2 and Egr-1 expression, whereas Egr-2 expression is greatly increased.
Brutkiewicz et al. (1995)IL-2T cellConsistent with these results, IL-2 production by the mCD1.1-specific T cell hybridoma DN32.D3 was induced by thymocytes from normal mice or mice with a homozygous deletion of the TAP1 gene, but not by thymocytes from mice with a homozygous deletion of the beta 2m gene.
Cho et al. (2000)interleukin 2T cellLike antigen-induced memory T cell differentiation, the homeostasis-driven process requires T cell proliferation and, initially, the presence of appropriate restricting major histocompatibility complexes, but it differs by occurring without effector cell formation and without requiring interleukin 2 or costimulation via CD28.
Kaminski et al. (2009)IL-2T cellsIn fact, anti-CD28 treatment could still induce late-phase CD154 on anti-CD3-stimulated CD4 T cells expressing a mutated form of CD28 that not lead to the induction of IL-2.
Kim et al. (1992)IL-2T cellsThe activation of T cells by phorbol dibutyrate induced the expression of IL-2R but failed to induce the synthesis of IL-2 or the expression of cdc2-specific mRNA.
Harada et al. (2001)IL-2T cellsIn contrast to anti-CD3 and anti-CD28 Ab stimulation, PMA and anti-CD28 Ab stimulation failed to induce IL-2 production from CD28 Y189F transgenic T cells at any time point.
Chu et al. (1997)IL-2T cellsWe find that in the absence of added IL-12, B lymphomas expressing the alternate costimulatory ligand 4-1BBL can support the production of IL-2 and IL-4 but little detectable IFN-gamma by allogeneic CD28+ and CD28- T cells.
Takahashi et al. (1995)IL-2T cellsRT-PCR analysis revealed that CD4+ T cells from the SEB-sensitive mice expressed significant levels of IFN-gamma, IL-2, IL-4 and IL-10 mRNA, while those from the tolerant mice exhibited significant levels of IFN-gamma but not IL-2 or IL-4 mRNA.
Ren et al. (2008)IL-2T cellUnexpectedly, DC(ap) supported T cell activation to a similar extent as normal DC in vitro, leading to proliferation and IL-2 production, except that DC(ap) did not support T cell production of IFN-gamma.
Brooks and Vitetta (1986)IL 2T cellA second set of neoplastic B cell clones derived from the AKR 225 lymphoma did not respond to rIL 2 even though they expressed receptors for IL 2 and could be induced by T cell supernatant to secrete IgM, thus indicating that expression of IL 2R is not the sole requirement for IL 2 responsiveness.
Gorczynski et al. (2000)IL-2T cellsDC incubated with ODN-1 to MD-1 did not stimulate IL-2 or IFN-gamma production, but generated cells able to suppress, in a second culture of fresh DC plus allogeneic T cells, production of IL-2 and IFN-gamma.
Takahashi et al. (1995)IL-2T cellsRT-PCR revealed that the SP CD4+ T cells did not generate IL-2 mRNA, while the PP CD4+ T cells expressed significant levels of IFN-gamma, IL-2, IL-4, and TGF-beta mRNA.
Stafford-Brady et al. (1989)interleukin-2T cellsTriggering of the T-cell receptor in these lpr T cells does not lead to translocation of protein kinase C or phosphorylation of CD3, interleukin-2 production, or proliferation, whereas a combination of phorbol ester and calcium ionophore does.
Tsukada et al. (1991)interleukin-2T cellsThe production of interleukin-2 (IL-2) and IL-3 but not IL-4 was observed in both T cells mediating only DTH and those mediating DTH and ACR.
Yu et al. (2003)IL-2T cellSolid-phase EFNB2 along with suboptimal anti-CD3 strongly stimulated T cell proliferation, with concomitant augmentation of IFN-gamma but not IL-2 or IL-4 secretion.
Galvin et al. (1992)IL-2T cellStimulation of T cell bulk cultures resulted predominantly in the production of IL-2 and not of IL-4.
Dumont (1987)IL 2T cellsResponsiveness of lpr/lpr T cells could not be restored with IL 1, IL 2, or both.
Oldstone and Madhani (2009)IL-2T cellsWhat is known is that by 9 days after a persistent LCMV infection is initiated in adult mice, T cells become unresponsive; that is, they fail to or poorly lyse virus-infected targets and do not make the positive immune regulators IL-2, interferon-?
Gaglia et al. (2001)IL-2T cellHowever, we have noted that nontransfected CHO cells can themselves provide a low-level B7/CD28 independent costimulatory signal for CD3-mediated murine T cell activation and IL-2 production.
Byun et al. (2010)IL-2T lymphocytesGISF (50 and 150 kGy) augmented immune responsiveness via activation of NK cells, T lymphocytes proliferation, NO production, and cytokine level, such as IL-6, IL-2, IL-12, IFN-gamma, TNF-alpha, as compared with NISF, which strongly suggested that GISF significantly augmented an important element of all aspects of the innate and adaptive immune system.
Remer et al. (2009)IL-2T cellAlthough dendritic cells readily upregulated maturation and activation markers in response to K88 stimulation, accompanied by secretion of interleukin (IL)-12, IL-6, IL-10, and tumour necrosis factor, restimulation of T cells from mice having received EcN-K88 with K88-loaded dendritic cells did not result in detectable T cell proliferation and IL-2 secretion, but rather induced an IL-10 bias.
Lynch et al. (2010)IL-2T cellsAlthough pTHgagC did not induce Gag-specific CD4+ T cells that produced IL-2, a high cumulative magnitude of 390 sfu/106 splenocytes Gag-specific CD4(13) and GagCD4(17) T cells producing IL-2 was detected in response to a DNA prime BV VLP boost.
Apostolaki and Williams (2004)interleukin 2T-cellFurthermore, a lack of CD25 expression on dividing cells suggested that EtxB-mediated T-cell clonal expansion may occur without a sustained requirement for interleukin 2.
White et al. (1996)IL-2T cellsIn contrast to observations that beta 2m-/- mice are resistant to many infectious diseases by compensatory mechanisms involving non-class I-restricted T cells, we found that beta 2m-/- mice failed to be protected against P. berghei SPZ, although immunization with attenuated SPZ induced production of IL-2, INF-gamma, anti-circumsporozoite protein IgG, and proliferative T cells.
Chiang et al. (2000)interleukin-2T-cellHere we show that T cells that are deficient in the adaptor molecule Cbl-b (ref. 3) do not require CD28 engagement for interleukin-2 production, and that the Cbl-b-null mutation (Cbl-b(-/-)) fully restores T-cell-dependent antibody responses in CD28-/- mice.