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

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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.
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.
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.
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.
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.
Waldmann et al. (1985)IL-2T-cellIn human T-cell lymphotropic virus-I infected cells, the Mr 42,000 long open reading frame protein encoded in part by the pX region of this virus may act as a transacting transcriptional activator that induces IL-2 receptor gene transcription, thus providing an explanation for the constant association of IL-2 receptor expression with adult T-cell lymphotropic virus-I infection of lymphoid cells.
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).
Wieder et al. (1990)IL-2T-cellsTo amplify very low levels of IL-2 mRNA, sequential reverse transcription and polymerase chain reaction (RT-PCR) of T cell mRNA were used to demonstrate the capacity of the calcium signal (ionomycin) to promote low-level IL-2 transcription in normal human T-cells without additional signals.
Ferguson et al. (2001)IL-2 geneT-cellShortly after T-cell stimulation, transcription of the IL-2 gene is upregulated.
Tessier et al. (2002)interleukin-2T-cellWe assessed the implication of these PLA(2) isoforms in transcription of the interleukin-2 (IL-2) gene, involved in T-cell proliferation.
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.
Becker et al. (1995)IL-2T cellsAnergy is a mechanism of T-lymphocyte tolerance induced by antigen-receptor stimulation in the absence of costimulation, whereby T cells exhibit a defect in antigen-induced transcription of the interleukin 2 (IL-2) gene.
Granelli-Piperno (1992)IL-2T lymphocytesCyclosporin A (CsA) and FK506 inhibit the production of IL-2 in T lymphocytes at the level of gene transcription.
Evans et al. (1992)IL-2T-cellFrom these data we conclude that, in human T-cells, RB phosphorylation is not directly associated with T-cell receptor-mediated events, but requires the interaction of IL-2 and new gene transcription following IL-2 stimulation.
Krönke et al. (1985)IL-2T cellsAlthough silent in resting T cells, the genes encoding c-myc and the interleukin 2 (IL-2) receptor were induced early, preceding gamma interferon (IFN-gamma), IL-2, and transferrin receptor gene transcription.
Hurez et al. (2003)IL-2T cellThus, there is intrinsic variability in clonal T cell populations that restricts IL-2 commitment, and prolonged engagement with mature DCs is necessary, but not sufficient, for IL-2 gene transcription.
Lewis et al. (1993)IL-2T cellTherefore, the mechanism by which inhibitors of PDE-III and PDE-IV affect T cell proliferation is not likely to involve suppression of IL-2 mRNA transcription.
Mouzaki et al. (1993)IL-2T cellsIn the present study, analysis of the interleukin-2 (IL-2) gene activation shows that naive human helper T cells (cord blood CD4+ T cells, adult CD4+CD45RO- T cells) regulate IL-2 transcription by a mechanism involving both a silencer and an activator acting on the purine-rich IL-2 promoter elements (NF-AT binding sites).
Kroemer et al. (1991)IL-2T lymphocytesIn the peripheral lymphoid organs, IL-2 is produced by a defined population of mature CD4+ T lymphocytes in which the IL-2 gene is transcribed or silenced, depending on the combination of antigenic and nonspecific activation signals to which the cell is exposed.
Paliogianni et al. (1993)IL-2 geneT cellWe have previously shown that prostaglandin E2 and other cAMP elevating agents inhibit the nuclear transcription of the human IL-2 gene by interfering with a Ca(2+)-sensitive T cell signal transduction pathway.
Garrity et al. (1994)Interleukin-2T cellsInterleukin-2 (IL-2) transcription is developmentally restricted to T cells and physiologically dependent on specific stimuli such as antigen recognition.
Garrity et al. (1994)IL-2T cellsWe conclude that binding activities of all classes fail to stably occupy their cognate sites in IL-2, except following activation of T cells, and that specificity of IL-2 transcription is enforced at the level of chromosomal occupancy, which appears to be an all-or-nothing phenomenon.
Lafont et al. (1998)interleukin-2T cellsIt has been shown that stimulation of lymphoid cells causes the activation of the extracellular signal-regulated-2 (ERK-2) which activates nuclear factor of activated T cells (NF-AT), a transcription factor involved in the regulation of interleukin-2 (1L2) gene transcription.
Paliogianni and Boumpas (1996)interleukin 2T cellsProstaglandin E2 inhibits the nuclear transcription of the human interleukin 2, but not the Il-4, gene in human T cells by targeting transcription factors AP-1 and NF-AT.
Lindstein et al. (1989)IL-2T cellThis pathway does not directly affect the steady-state messenger RNA level, transcription, or messenger RNA half-life of other T cell activation genes, including c-myc, c-fos, IL-2 receptor, and the 4F2HC surface antigen.
Junger et al. (1997)IL-2 mRNAT-cellHuman Jurkat T-cells were used to study the effects of HTS on T-cell signal transduction, IL-2 mRNA transcription, and IL-2 expression.
Junger et al. (1997)IL-2 mRNAT-cellHTS alone does not result in IL-2 mRNA transcription, IL-2 expression, or T-cell proliferation.
Baroja and Ceuppens (1987)IL-2T-cellsPrecise measurement of IL-2 production in vitro is hampered by binding of IL-2 to IL-2 receptors on activated T-cells which results in IL-2 consumption.
Lum et al. (1986)IL-2T cellThe present studies indicate that during T cell activation, induction of IL-2 mRNA transcription and IL-2 receptor expression precede the transcription of Tf mRNA and expression of Tf receptors, respectively.
Noma et al. (1984)IL2CTCOur study focuses on the effect of Bestatin on interleukin 2 (IL2) sensitivity of IL2-dependent cultured T cells (CTC) and on IL2 production by human peripheral blood mononuclear cells (PBM).
Shaw et al. (1988)IL-2 mRNAT lymphocytesMechanisms regulating the level of IL-2 mRNA in T lymphocytes.
Scheer et al. (2003)interleukin-2T lymphocytesCyclosporin has a specific effect, because it inhibits interleukin-2 transcription and, consequently, the specific activation of T lymphocytes.
Mastro et al. (1991)IL-2T lymphocytesUnder conditions of TPA treatment in which protein kinase C was chronically reduced in T lymphocytes, IL-2 production was greatly depressed as were the level of IL-2 mRNA and [3H]thymidine incorporation.
Lopez et al. (1998)IL-2 RNAT cellThese findings show that human breast cancer tumor-induced repression of IL-2 RNA translation is the basis of failure of TIL to express the IL-2 receptor and subsequent T cell hyporesponsiveness.
Plana et al. (1991)IL2T cellsAn increased IL2 secretion in T cells cultured with PMA plus 134-2C2 mAb was observed and Northern blot analysis showed that the mAb 134-2C2 acts synergistically with PMA favoring the induction of both IL2 and interferon-gamma mRNA synthesis, as well as the enhancement of IL2 receptor and transferrin receptor mRNA expression.
Nguyen et al. (2010)interleukin-2T cellsNFAT and AP-1 proteins induce interleukin-2 (IL-2) transcription in stimulated T cells, but the contributions of individual members of these activator families to synergistically activating IL-2 transcription is not known.
Nguyen et al. (2010)IL-2T cellsA region of NFATc2 C-terminal of the DNA binding domain was necessary and sufficient for interaction with cJun in the absence of DNA, and this same region of NFATc2 was required for the synergistic activation of IL-2 transcription in T cells.
Nguyen et al. (2010)IL-2T cellsThese studies show that a previously unidentified interaction between human NFATc2 and cJun is necessary for synergistic activation of IL-2 transcription in T cells.
Fessler et al. (1996)IL-2T cellIn T cells stimulated through the T cell receptor (TCR), both cyclosporine (CsA) and glucocorticoids (GC) inhibit the transcription of the IL-2 gene.
Huang et al. (1992)cell-IL-2T cellThe T cell-IL-2 activity, expressed as a T cell-IL-2 activity score (calculated as the logarithm of the serum IL-2 U/ml divided by the logarithm of the IL-2 secretion U/ml, in vitro) was significantly increased in elderly non-responders after influenza vaccination (mean +/- 1 SD: 1.4 +/- 0.51) compared with elderly (0.44 +/- 0.13) and younger responders (0.3 +/- 0.2).
Eriksen et al. (2001)IL-2T cellsWe show that (1) STAT3 (a transcription factor known to regulate IL-2Ralpha transcription) is constitutively tyrosine-phosphorylated in SS tumor cells, but not in non-malignant T cells; (2) STAT3 binds constitutively to a STAT-binding sequence in the promotor of the IL-2Ralpha gene; (3) the Janus kinase inhibitor, tyrphostine AG490, inhibits STAT3 activation, STAT3 DNA binding, and IL-2Ralpha mRNA and protein expression in parallel; and (4) tyrphostine AG490 inhibits IL-2 driven mitogenesis and triggers apoptosis in SS tumor cells.
Koizumi et al. (1989)IL-2T-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.
Boussiotis et al. (1997)IL-2T cellMaintenance of human T cell anergy: blocking of IL-2 gene transcription by activated Rap1.
Boussiotis et al. (1997)IL-2T cellsForced expression of low amounts of Rap1-GTP in Jurkat T cells recapitulated the anergic defect and blocked T cell antigen receptor (TCR)- and CD28-mediated IL-2 gene transcription.
Boussiotis et al. (1997)IL-2T cellTherefore, Rap1 functions as a negative regulator of TCR-mediated IL-2 gene transcription and may be responsible for the specific defect in IL-2 production in T cell anergy.
Lewis et al. (1986)IL-2T cellsIn contrast, IL-2, IL-2-R, and T3 delta chain mRNA levels were kinetically and quantitatively similar in neonatal and adult T cells.
Marcoulatos et al. (1996)IL-2 geneT cellNFAT acts at the antigen receptor response element-2 (ARRE-2) sequence in the IL-2 enhancer and is the nuclear target of T cell stimulation signals and the immunosuppressant drugs cyclosporine and FK506, which are potent inhibitors of IL-2 gene transcription.
Steenbakkers et al. (1999)IL-2T cellsFollowing the anergic stimulus, T cells failed to proliferate upon restimulation as a result of a lack of interleukin-2 (IL-2) gene transcription.
Tao et al. (1996)IL-2 geneT cellThese results have localized the effect of T2 to a step in the T cell activation cascade after initial second messenger generation, tyrosine phosphorylation and protein kinase activation, but before IL-2 gene transcription.
Sakitani et al. (1987)IL-2T cellStudies on distinct HTLV-1-infected T cell clones that differed in numbers of high-affinity IL-2R, showed that the extents of increase in mRNA expression by IL-2 were correlated with the number of high-affinity IL-2R.
Qiu and Kao (2003)interleukin-2T-cellTriptolide inhibits lymphocyte activation and T-cell expression of interleukin-2 at the level of transcription.
Paliogianni et al. (1993)IL-2 geneT lymphocytesThese results suggest that in human T lymphocytes both Dex and CsA inhibited IL-2 gene transcription through interference with transcription factors AP-1 and NF-AT.
Morvan et al. (1994)IL-2 mRNAT cellsIL-2 mRNA was first detected in activated Jurkat T cells.
Luria et al. (1991)IL-2 geneT-cellThese findings, and others described herein, suggest that the virally encoded Nef protein interferes with a signal emanating from the T-cell receptor complex that induces IL-2 gene transcription.
Weissman et al. (2000)IL-2T cellsUnlike in vitro studies, CCR5 was coexpressed with CD45RA and CXCR4 on CD4+ T cells after IL-2 therapy.
Akbar et al. (1991)IL2T cellsSignificantly, the CD4+CD45RA+ T cells synthesized two- to threefold more mRNA for IL2 than the CD4+CD45R0+ subset, while the CD4+CD45R0+ T cells synthesized mRNA for IL4 and interferon-gamma exclusively.
Migone et al. (2001)IL-2T cellsThe results of this study show that DUB-2 is expressed in human T-cell lymphotropic virus-I (HTLV-1)-transformed T cells that exhibit constitutive activation of the IL-2 JAK/STAT (signal transducers and activators of transcription) pathway, and when expressed in Ba/F3 cells DUB-2 markedly prolonged IL-2-induced STAT5 phosphorylation.
Woodside and McIntyre (1998)IL-2T lymphocytesHowever, there has been no direct demonstration that activator protein-1 is involved in CD28-dependent costimulation of IL-2 gene transcription in freshly isolated naive and memory human T lymphocytes.
Woodside and McIntyre (1998)IL-2T lymphocyteScrape loading thus provides an efficient mechanism for intracellular incorporation of macromolecules, and the first direct evidence that c-Fos and c-Jun are involved in transcription of the IL-2 gene within its correct chromosomal context, in resting human T lymphocyte subpopulations.
Schwarz et al. (1993)IL2 geneT-cellThese results suggest that IL-4 may regulate development and function of T-cell subsets involved in cell-mediated immunity in part by inhibiting factors required for transcription of the IL2 gene.
Hodgkin et al. (1987)lymphokineT cellThe process of lymphokine release can be divided into 4 steps: Antigen binds to the T cell; a signal is transferred to the cell nucleus; transcription of lymphokine-encoding mRNA occurs; and intact lymphokine is synthesized and secreted.
Bulfone-Paus et al. (1997)IL-2T cellIn order to screen for functional differences between IL-2 and IL-15 with respect to the control of T cell functions, we have stimulated human T lymphoblasts (hTBl) with IL-2 and/or IL-15 and have assessed the resulting changes in the following parameters: T cell proliferation; expression of various relevant surface markers; cytokine and receptor (alpha-chain) transcription; and IL-2 and IL-15 activity.
Jaalouk et al. (2006)IL-2T-cellBACKGROUND: T-cell activation leads to signaling pathways that ultimately result in induction of gene transcription from the interleukin-2 (IL-2) promoter.
Roth and Dröge (1991)interleukin 2T cellsHere we report that high but physiologically relevant concentrations of lactate increase the expression of interleukin 2 (IL 2)-specific mRNA and the production of IL 2 activity in cultures of mitogenically stimulated T cells.
Motmans et al. (1996)interleukin-2T cellsThis technique was applied to quantify tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma) and interleukin-2(IL-2) mRNA levels in human T cells transfected with the corresponding genes.
Beadling and Smith (2002)IL-2 geneT cellsInstead, in the mid '80s it was found that the activation of co-stimulatory molecules like CD28 expressed by T cells via ligands such as B7 expressed by antigen presenting cells (APC), deliver additional signals that synergize with those emanating from the TCR, and result in maximal IL-2 gene transcription [23].
Marcoulatos et al. (1998)IL-2 geneT cellNFAT acts at the antigen receptor response element-2 (ARRE-2) sequence in the IL-2 enhancer and is the nuclear target of T cell stimulation signals and the immunosuppressant drugs cyclosporine (Sandimmune) and FK-506 (tacrolimus), which are potent inhibitors of IL-2 gene transcription.
Yang et al. (2002)IL-2T lymphocytesWe have shown previously that the activated PPARgamma is a profound inhibitor of IL-2 transcription in human T lymphocytes.
Holländer (1999)IL-2T cellsProduced exclusively in T cells, IL-2 transcription and synthesis occurs only after appropriate cellular activation via the clonotypic antigen-receptor and co-stimulatory molecules.
Sunder-Plassmann et al. (1996)interleukin-2T cellsSingle human T cells stimulated in the absence of feeder cells transcribe interleukin-2 and undergo long-term clonal growth in response to defined monoclonal antibodies and cytokine stimulation.
Pan et al. (2004)interleukin-2 geneT lymphocytesMyocyte enhancer factor 2 mediates calcium-dependent transcription of the interleukin-2 gene in T lymphocytes: a calcium signaling module that is distinct from but collaborates with the nuclear factor of activated T cells (NFAT).
Pan et al. (2004)interleukin-2 geneT cellThe second messenger calcium plays an essential role in the T cell receptor-mediated signal transduction pathways leading to transcription of the interleukin-2 gene.
Pan et al. (2004)IL-2T cellsDown-regulation of MEF2 by RNA interference in primary human T cells led to the inhibition of endogenous IL-2 transcription.
Woerly et al. (1996)IL-2T lymphocyteThe immunosuppressive macrolide rapamycin inhibits cytokine-driven proliferation of lymphocytes, acting at a later stage of T lymphocyte activation than the related compound FK506 or cyclosporin, which block IL-2 transcription.
Turka et al. (1991)IL-2T cellEarly events in T cell activation, as assessed by steady-state mRNA levels of c-myc, IL-2, c-myb, histone, and cdc2 kinase, as well as surface IL-2 receptor expression, were unaffected.
Lewis et al. (1991)IL-2 mRNAT cellsIn addition, IFN-gamma and IL-2 mRNA were significantly more abundant than IL-4 mRNA in activated neonatal CD4+CD8- thymocytes and CD4+ T cells, as well as adult CD4+ CD45R- T cells.
Gruters et al. (1991)IL2T cellIn accordance with observations by Verweij, Geerts and Aarden on the CD28 co-stimulatory activation of IL2 transcription via an NF-kB-like activity, stimulation of the CD2, CD28 and CD44 accessory molecules was tested to mimick physiological activation signals independent of T cell receptor triggering. mAb directed against CD2 and CD44 only marginally induced the LTR.
de la Rosa et al. (2004)IL-2TregIL-2 has been implicated in the generation and maintenance of Treg, however, a functional contribution of the IL-2 receptor during suppression is thus far unknown.
Bendiksen and Rekvig (2004)IL-2T cellsWhile T-antigen did not reactivate anergic T cells, proliferation and upregulation of IL-2 gene transcription was initiated by stimulation with antigen, costimulation and IL-2 added to the cultures.
Bendiksen and Rekvig (2004)IL-2T-cellRequirements for the reactivation of anergic T cells were analysed by the ability of antigen and interleukin-2 (IL-2) or IL-15 to increase T-cell proliferation and IL-2 transcription.
Kryworuchko et al. (2003)IL-2T cellsIn CD4 T cells, we have observed previously that viral envelope (env) glycoproteins induce IL-2 unresponsiveness and the down-regulation of the three chains making up the IL-2R (alpha, beta, gamma) in vitro.
Hughes and Pober (1993)IL-2T cellWe therefore examined the effects of EC on T cell nuclear factors known to regulate IL-2 transcription, including c-jun and c-fos-two components of the transcription factor AP-1, NFAT, and others.
Okochi et al. (2005)IL-2T cellsTob is a member of an emerging family of anti-proliferative proteins that suppress cell growth when over-expressed. tob mRNA is highly expressed in anergic T cells and over-expression of Tob suppresses transcription of interleukin-2 (IL-2) through its interaction with Smads.
Lafont et al. (1999)IL-2T lymphocytesEvidence for a p21(ras)/Raf-1/MEK-1/ERK-2-independent pathway in stimulation of IL-2 gene transcription in human primary T lymphocytes.