Viewing negative mentions of negative regulation in T cells

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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.
Chao et al. (2007)CD25 mRNAT lymphocytesCONCLUSION(S): This study demonstrates the effectiveness of the coculture model to study fetomaternal interactions and provides evidence that fetal cells may contribute to the control of maternal local immunity and that the decreased expression of CD25 on decidual T lymphocytes is not through the reduced CD25 mRNA level.
Hill et al. (2007)IL-4T cellHere, we show that IL-4 only enhances the expansion of autoreactive CD4 T cells during lymphopenia and that neither the presence of islet IL-4 nor IL-4 deficiency affects T cell expansion significantly under conditions of immunosufficiency.
Grote et al. (2004)CCN1T-cellsDecoy oligonucleotides to Egr-1, but not to nuclear factor of activated T-cells or cAMP response element binding protein, abolished the stretch-induced transcription of CCN1.
Hahn et al. (2004)AHRT cellsVgamma4(+) gammadelta T cells strongly suppressed AHR; their depletion relieved suppression when initiated before challenge, but not before sensitization, and they suppressed AHR when transferred before challenge into sensitized TCR-Vgamma4(-/-)/6(-/-) mice.
Endsley et al. (2002)CD25T cellsWhen incubated with live BHV-1, depletion of CD4+ T cells depressed the expression of CD25 by CD8+ T cells, but not gammadelta T cells.
Reichardt et al. (2007)L-selectinT cellsB cells induce substantial proliferation but, contrary to DCs, no loss of L-selectin in T cells.
Kumagai et al. (1988)TFR mRNAT cellsThe early accumulation of TFR mRNA in PDB/ionomycin-stimulated T cells seemed, in part, independent of the interaction of IL-2 with its own receptor, because TFR mRNA was detectable as early as 1 hr after stimulation and addition of cycloheximide before addition of PDB/ionomycin did not abolish the PDB/ionomycin-induced accumulation of TFR mRNA.
Young and Matthews (1995)alpha-chain interleukin-2 receptorT cellsWhile the proportions of splenic CD4+ and CD8+ T cells isolated from control and PCPA-treated mice were similar, the level of expression of the alpha-chain interleukin-2 receptor (IL-2R) was reduced on splenic CD4+ cells but not on CD8+ cells.
Prochorec-Sobieszek et al. (2008)pan-T antigensT-cellIn the former no loss of expression of any pan-T antigens was observed, in the latter typical abnormalities of pan-T-cell antigens were noted.
Lin et al. (2007)interleukin (IL)-7RalphaT cellThe PD-1+ HP cell population, which peaked in frequency at day 21, was dysfunctional in that it failed to produce interferon gamma or tumor necrosis factor alpha on T cell receptor (TCR) stimulation, had down-regulated expression of interleukin (IL)-7Ralpha, IL-15Rbeta, and Bcl-2, and reacted with Annexin V, which is indicative of a preapoptotic state.
Doh and Irvine (2006)IFN-gammaT cellsIn contrast, T cells interacting with activation sites patterned to preclude centralized clustering of TCR ligand failed to form stable contacts with activation sites, exhibited aberrant PKC- clustering in a fraction of cells, and had significantly reduced production of IFN-gamma.
Datta et al. (2006)AKTT-cellThe inhibition of T-cell chemotaxis correlated with reduced AKT/PKB but not ERK activation following exposure to the chemokine CXCL-12/SDF-1.
Wong et al. (2005)T cellsPre-treatment of T cells with NO or a cGMP agonist decreased binding to recombinant endothelial adhesion molecules.
Park et al. (2001)STAT6T cellsImportantly, STAT6 phosphorylation following IL-4 stimulation was not decreased in anti-CD28-uncostimulated T cells.
Cramer and Frelinger (2001)HLA-BT cellsIn contrast to T cells and Hela cells, HLA-A and HLA-B molecules are not downregulated nor are other class I molecules increased.
Cramer and Frelinger (2001)HLA-AT cellsIn contrast to T cells and Hela cells, HLA-A and HLA-B molecules are not downregulated nor are other class I molecules increased.
Takahashi et al. (1999)DTHT cellThe present study showed that DTH was not suppressed in splenectomized mice, but was inhibited in splenectomized mice transferred with a primed CD4+ T cell-containing fraction of spleen cells.
Shimoda et al. (1998)PHAT lymphocyteOn the other hand, thunberginol A significantly suppressed T lymphocyte proliferation stimulated by concanavalin A (Con A), but did not suppress phytohemagglutinin (PHA).
Shimoda et al. (1998)phytohemagglutininT lymphocyteOn the other hand, thunberginol A significantly suppressed T lymphocyte proliferation stimulated by concanavalin A (Con A), but did not suppress phytohemagglutinin (PHA).
Ben-Amor et al. (1996)CD3T cellAt the dose used, anti-CD3 resulted neither in T cell depletion nor in down-modulation of the CD3/T cell receptor (TCR) complex.
Maiese et al. (1995)cellT-cellAll pan-T-cell-associated antigens studied were expressed within a narrow range of average values (54 - 64%), and no loss of individual T-cell antigens was observed in any case.
Hamrell et al. (1995)V0T cellsThus, V0 was markedly reduced in acute viral myocarditis in the absence of tissue disruption or hypertrophy, but not if T cells were absent.
Todd et al. (1994)V beta 6T cellWe show here that introducing cells expressing the endogenous superantigen Mls 1a into an Mls 1b environment results in the induction of an anergic state with little or no depletion of V beta 6/CD4+ T cell from the peripheral T cell repertoire.
Liebers et al. (1994)cellT cellsHLA-DR on T cells (CD3+), and CD25 as well as CD23 expression, could be significantly enhanced after antigen-specific stimulation in patients but not in controls, whereas alpha/beta-T-cell-receptor expression was significantly reduced in patients.
Morahan et al. (1991)CD8 moleculesT cellsPersisting T cells had not down-regulated either their antigen-specific receptors or their CD8 molecules.
Koizumi et al. (1989)c-mycT-cellKH-2 cells are integrated by HTLV-I proviral DNA and expressed mRNA for c-myc, IL-2 receptor alpha-chain (IL-2R alpha), and T-cell receptor beta-chain (TCR beta) while it did not express IL-2 mRNA. 1,25(OH)2D3 and dexamethasone did not suppress the mRNA levels of HTLV-I, IL-2R alpha or TCR beta but reduced the c-myc mRNA level.
Börgermann et al. (2007)HLA-DRT-cellsIn contrast, HLA-DR expression on T-cells was unchanged, whereas HLA-DR expression on B-cells did not decrease before the 2nd day after CPB (152 +/- 3 MCF vs. 170 +/- 2 MCF preoperatively, P < 0.001).
Kita et al. (1990)IL-2T-cellT-cell growth factor activity of IL-2 preparation prepared on day 28 of treatment as determined by HT-2 cell proliferation was reduced by about 40% in the presence of anti-murine IL-4 monoclonal antibodies, while control IL-2 activity was not reduced.
Tsitoura et al. (1997)TGF-betaT cellsFurthermore, exposure of the T cells to the wild-type HA peptide under conditions that induce T-cell anergy resulted in the secretion of TGF-beta, and subsequent antigenic rechallenge was unable to override this signal and down-regulate TGF-beta production.
Nesburn et al. (2007)CD4T cellsConjunctiva-derived CD4(+) CD25((Bright+)) T cells, but not CD4(+) CD25((low)) T cells, efficiently suppressed HSV-specific CD4(+) and CD8(+) T(eff) cells.
Chien et al. (2001)PKCT cellsThe results indicated that, (1) alkalinization was induced by PHA or PMA in T cells; the results of alkalinization was PKC-dependent and Ca(2+)-independent, (2) in PKC down-regulated T cells, PHA induced acidification; this effect was enhanced by pre-treating the cells with the Na(+)/H(+) exchange inhibitor, 5-(N,N-dimethyl)-amiloride, (DMA, 10 microM, 20 min), (3) the acidification was dependent on the Ca(2+) influx and blocked by removal of extracellular calcium or the addition of the inorganic channel blocker, Ni(2+), and (4) Thapsigargin (TG), a Ca(2+)-ATPase inhibitor, confirmed that acidification by the Ca(2+) influx occurred in T cells in which PKC was not down-regulated.
Rayamajhi et al. (2010)IFNGRT cellsdoes not reduce IFNGR expression in T cells, the integration of IFN-??
Zheng et al. (2001)FasT cellsAlthough proliferative responses were significantly impaired, expression of Fas and activation-induced cell death was unaffected in T cells obtained from these different mice.
Korthäuer et al. (2000)GRP1T cellsHowever, GRP1-transduced T cells were not stable and rapidly lost GRP1 expression.
Yang et al. (2003)NF-kappaBT cellsMolecular investigation indicated that carvedilol specifically downregulated NF-kappaB but not activator protein 1 DNA-binding activity in activated T cells.
Liegler et al. (2001)CD4T-cellCONCLUSIONS: Primary isolates from patients showing virologic rebound without net CD4 T-cell loss during continued therapy are as cytopathic as PI-sensitive isolates with equivalent input infectious titer.
Alonso et al. (2002)VHXT cellVHX expression was not induced by T cell activation, but decreased somewhat at later time points.
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.
Murray et al. (1990)IL2T cellsSimilar levels of IL2 mRNA were present in the CD4+ T cells of lpr and MRL/n mice, demonstrating that these cells are not defective in IL2 production in vivo.
Camacho et al. (2002)aryl hydrocabon receptorT cellThe resistance to TCDD-induced decrease in T cell responsiveness to SEA seen in Fas- and FasL-mutant mice was neither due to decreased aryl hydrocabon receptor (AhR) expression nor to altered T cell responsiveness to SEA.
Oishi et al. (2000)CXCR4T cellsUpregulation of CCR4 and CCR5 expression but no decrease in CXCR4 expression on CD4+ T cells were obtained in peripheral blood from African adults with progression of the disease.
Appasamy et al. (1997)CD8T cellBestatin did not downregulate expression of CD8 by a mature CD8+ T cell clone.
Schmitt et al. (1994)IL-4T cellThese data were confirmed by time-course experiments which revealed that the delayed addition of IL-4 to IL-12-primed T cell cultures resulted in a gradual restoration of IFN-gamma production whereas in parallel the secretion of IL-4 was not reduced over a wide period of delay (6-72 h).
Singh and Lebedeva (1994)IgGT cellFurthermore, IL-1Ra treatment of B plus T cell co-cultures derived from diseased MRL/lpr mice was able to significantly suppress IgG production, whereas, IL-1Ra treatment of B plus T cell co-cultures derived from pre-disease MRL/lpr mice demonstrated virtually no suppression in IgG production.
Grant et al. (2006)NF-kappaBFoxp3T cellsDeletion of the carboxyl-terminal forkhead (FKH) domain, critical for nuclear localization and DNA-binding activity, abrogated the ability of Foxp3 to suppress NF-kappaB activity in HEK 293T cells, but not in Jurkat or primary human CD4+ T cells.
Teague et al. (1997)Bcl-2T cellsIf during this time period the T cells are incubated with rIL-6, Bcl-2 expression is not down-regulated.
Lockhart et al. (2001)TCRzetaT cellsExposure of normal T cells to relative ischemia or heat shock, or culture in medium without IL-2, did not significantly reduce expression of TCRzeta compared with CD3epsilon.
Waldmann et al. (1975)immunoglobulinT cellIn addition, in control studies no such suppression of immunoglobulin synthesis was seen when normal cells were co-cultured with lymphocytes from unrelated normals, patients with isolated IgA deficiency, patients with chronic lymphocytic leukemia or patients with the Sezary syndrome, a T cell leukemia nor were they inhibited when incubated with T cells from unrelated normals.
Schindler et al. (2007)NFATT cellsFurthermore, the F191H/R changes neither affected the levels of interleukin-2 receptor expression and apoptosis of HIV-1-infected primary T cells nor reduced Nef-mediated induction of NFAT.
Zhang et al. (2000)SHP-1 proteinT-cellWe found that SHP-1 protein was not detectable or greatly diminished in most (six of seven) T cell lines derived from various types of T cell lymphomas and all (eight of eight) cutaneous T-cell lymphoma tissues with a transformed, large-cell morphology.
Boitard et al. (1982)InsulinT lymphocyteInsulin release was suppressed by the OKT3+ (T lymphocyte-enriched) subset, but not by the OKT3- (T lymphocyte-depleted) subset.
Najafian et al. (2003)myelin oligodendrocyte glycoproteinCD28T cellsIn vitro, CD8+CD28- but not CD8+CD28+ T cells suppress IFN-gamma production of myelin oligodendrocyte glycoprotein-specific CD4+ T cells.
Uckun et al. (1992)B43 monoclonal antibodyB43 monoclonal antibodyT-cellIn contrast, neither unconjugated B43 monoclonal antibody nor the anti-T-cell immunotoxin G17.2 (anti-CD4)-PAP decreased the incidence of paraplegia or improved EFS.
Racioppi et al. (1990)c-fosmAb Q5/6T lymphocytesThe results show that in T lymphocytes the expression of c-fos and early c-myc mRNA was unaffected by mAb Q5/6, whereas the c-myb and N-ras mRNA levels were strongly diminished as well as those of IL-2, IL-2R alpha, and IFN-gamma mRNA.
Zhao et al. (1998)IL-6T-cellPulsing normal spleen cell cultures with propanil for up to 8 h before T-cell activation resulted in reduced IL-6 but not IL-2 or IFN-gamma production.
Kondo et al. (1991)immunoglobulinT cellsHowever, in the cases in which only T cells were preincubated with IVIGs, immunoglobulin production was not suppressed.
DeKruyff et al. (1995)IL-4T cellsFirst, we found that the presence of IL-12 greatly reduced the development of IL-4 synthesis in resting but not activated memory CD4+ T cells.
Yamada et al. (1992)CD45RAT cellsAfter activation with PHA, adult CD45RA+ T cells began to express CD45RO and no loss of CD45RA expression had yet occurred at Day 3 post-stimulation.
Morahan et al. (1987)TCRT cellThese results indicate that TCR gene expression is not limited to a small subpopulation of T cell precursors.
Blanchard et al. (2004)IFN-gammaT cellMoreover, we show, in CD4(+) T cell blasts, that strong TCR clustering is required for neither TCR down-modulation nor optimal IFN-gamma production.
Zuñiga-Pflücker et al. (1989)CD4CD4T cellsSince F(ab')2 and Fab anti-CD4 fail to deplete CD4+/CD8- in adult mice, these results strongly argue that the absence of CD4+/CD8- T cells is not due to depletion, but rather, is caused by a lack of positive selection, attributable to an obstructed CD4-MHC class II interaction.
Gregory et al. (1986)MPIFT cellsMPIF was produced by alloantigen-stimulated, nylon wool-purified T cells and was not diminished by irradiation.
Brando et al. (2007)IFN-gammaT cellsHowever, inclusion of blocking anti-CD4(+) antibody during the in vitro restimulation ELISpot analysis failed to completely abolish IFN-gamma production, indicating that while CD4(+) T cells were the major source of IFN-gamma, other cell types also were involved.
Wonigeit et al. (1997)RT6T cellsTaken together, these findings demonstrate that the expression of RT6 is not restricted to T cells and is differently regulated in normal peripheral T cells, intestinal IEL, and NK cells.
Liu et al. (1998)CTLA-4T cellsBut patients with SLE had significantly increased percentages of CTLA-4-positive T cells compared with normal controls, implying at least that there was no apparent defective expression of CTLA-4 molecule in human lupus.
Bensinger et al. (2001)CD4T cellsIn contrast, CD4(+)25(+) T cells from MHC class II-deficient mice do not suppress responder CD4(+) T cells in vitro or in vivo.
Yager et al. (2010)CD8T cellVirus-specific CD8 T cell numbers and cytolytic function were not profoundly diminished with age.
McNab et al. (1996)VAP-1T-cellVAP-1--mediated adhesion was unaffected by T-cell activation with phorbol ester.
Chabannon et al. (1992)CD7T cellsWe conclude that CD7 expression is not restricted to T cells but is also expressed during early stages of myeloid differentiation.
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).
Merluzzi et al. (1982)TNP-LPST-cellAntibody responses to sheep red blood cells are augmented two to threefold in mice receiving NPT 15392 while T-cell independent antibody responses to TNP-LPS are unaffected.
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.
Shao et al. (2000)p53T lymphocytesTo study whether or not loss of p53 leads to genetic instability in normal cells in vivo, we have examined mechanisms of loss of heterozygosity (LOH) at the Aprt (adenine phosphoribsyltransferase) and flanking loci in normal fibroblasts and T lymphocytes of p53-deficient mice.
Turner et al. (1987)TNFT cellTNF production was not limited to T cells from autoimmune individuals, since the T cell tumor HUT78 and T cells purified from the peripheral blood of healthy individuals also made TNF.
Ermann et al. (2001)CD4T cellCD4(+)CD25(+) T cell-induced suppression, in this model, was not abrogated by blocking the B7-CTLA-4 pathway.
Tomizawa et al. (1985)VPFT lymphocytesThese results seem to suggest that the plasma from patients with MCNS in the active stage inhibits VPF production, but does not neutralize T lymphocytes derived VPF activity.
Blossom and Gilbert (2006)CD178T cellsTCAH attenuated AICD in CD4+ T cells by decreasing FasL (CD178) expression but not by altering Fas (CD95) expression or by interfering with Fas-signaling events following direct engagement of the Fas receptor.
Lang and Kastern (1989)RT6T lymphocyteThe gene for the T lymphocyte alloantigen, RT6, is not linked to either diabetes or lymphopenia and is not defective in the BB rat.
Papasavvas et al. (2000)CD4T cellAfter a median interruption of 55 days of therapy accompanied by rebound of virus, reinitiated therapy in 4 of 5 subjects resulted in suppression of 98.86% of plasma virus load by 21-33 days and no significant decrease in CD4 T cell percentage from baseline.
Turcotte and Lemieux (1989)IL-2T-cellThe depressed IL-2 utilization started to be observed about 1 to 2 weeks prior to the onset of the depressed IL-2 production and was not reversed by the addition of exogenous IL-2; thus implying that a lack of IL-2 utilization rather than a lack of IL-2 production could be directly responsible for the inhibition of T-cell proliferative responses to Con A in SC cultures of infected mice.
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.
Anderson and Fritsche (2004)CD4T-cellSurprisingly, (n-3) PUFA consumption did not reduce CD4(+) T-cell expansion.
Subauste et al. (1991)CD4T lymphocytesThe effector cells were shown to be CD8+ T lymphocytes, because the cytotoxicity was significantly inhibited by depletion of CD8+ T lymphocytes but not by depletion of CD4+ T lymphocytes.
Sasai et al. (2007)MGMTT cellsConversely, in human lung fibroblasts TIG3/T cells (TIG3 cells expressing hTERT) [14], neither SV40ER nor H-RasV12 suppressed MGMT expression (Figure 3B), suggesting the astrocyte-specific mechanisms of MGMT regulation.
Briken et al. (2000)CD1cT cellsFunctional studies using T cells specific for defined lipid antigens revealed that in contrast to CD1b-mediated antigen presentation, antigen presentation by CD1c was resistant to drugs inhibiting endosomal acidification and was independent of endosomal localization of CD1c.
Willey et al. (2003)CD4T cellsAlthough all of the vaccinated monkeys became infected, they displayed reduced postpeak viremia, had no significant loss of CD4(+) T cells, and have remained healthy for more than 15 months postinfection.
Le Rond et al. (2005)IDOT-cellTaken together, these findings show that the function and expression of IDO and HLA-G5 are not mutually influenced, but rather inhibit the T-cell alloproliferative response through two independent pathways.
Marracci et al. (2006)CD4T-cellLA treatment of Con A stimulated PBMC specifically removed CD4 from the T-cell surface, but not CD3.
Koenen et al. (2003)RapT-cellThe ability of Rap to promote apoptosis, which contributes to T-cell suppression, remained unaffected upon combination with FK506 or CsA.
Matsui and Arai (1993)IL-2T-cellThe suppression of T-cell proliferation did not necessarily parallel the level of interleukin-2 (IL-2) secretion, and was not restored by treatment with a calcium ionophore, indomethacin or IL-2.
Villa et al. (1999)Rag1T lymphocytesWe have recently shown that mutations that impair, but do not completely abolish the function of Rag1 and Rag2 in humans result in Omenn syndrome, an enigmatic form of combined immune deficiency characterized by oligoclonal, activated T lymphocytes with a skewed Th2 profile.
Kim et al. (1991)SEBT cellT cells bearing V beta 6 T cell receptor, which does not interact with SEB, were not reduced with SEB administration.
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.