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Click here for the function of IL2. Edit this page in Wiki Genes - IL2 or see Wiki Gene. Phosphatidyl inositol 3-kinase ( PI3K) is activated by IL-2. Paper-1240722. A specific inhibitor of TAK1 blocked production of IL-2. Paper-11445907. IL-2 and TNF have a synergistic effect on OPN expression. Paper-14376024. In addition, overexpression of TAK1 and TAB1 induced secretion of IL-2. Paper-11445907. IL-2 does not appear to modulate cytokine- induced HRPE IL-8 or MCP-1. Paper-895545. Raf-1 activity promotes IL-2 production in activated T lymphocytes. Paper-474124. Treatment of T lymphocytes with IL-2 promotes p56lck kinase activity. Paper-7193167. The proportion of IL2 secreting PBMC increased in three patients whose PSA fell. Paper-1634652. Induction of human lymphokine- activated killer cells by IFN-alpha and IFN-gamma. Paper-6164266. Therapy with interleukin-2 induces the systemic release of phospholipase-A2. Paper-454416. Moreover, IL-2- induced LAK activity was augmented by the concomitant addition of IL-7. Paper-1644608. However, IL-2- induced activator protein-1 ( AP-1) is oxidation-sensitive. Paper-8612699. CD80 induced higher levels of IL-2 promoter-enhancer activity compared to CD86. Paper-1492228. Thrombopoietin and interleukin-2 induce association of CRK with STAT5. Paper-8612674. This finding was likely due to IL-2- induced CCR5 expression on CD4+ thymocytes in FTOC. Paper-11536549. Crosslinking of the CD5 antigen on human T cells induces functional IL2 receptors. Paper-6630359. On the other side, HCS also enhances the lectin- induced production of IL2 by thymocytes. Paper-5135054. IL-2- induced IL-9 production by allergen-specific human helper T-cell clones. Paper-13372646. In these experiments, anti- LFA-1 mAb markedly up-regulated the lytic ability of IL-2-cultured PBL. Paper-7301119. These data show P-gp mediated transmembrane flux of IL-2 in T lymphocytes and HCT-8 cells. Paper-661406. Anti- beta 2m has no effect on mitogen- induced cell proliferation and IL 2 production. Paper-5133017. Shock waves increase T-cell proliferation or IL-2 expression by activating p38 MAP kinase. Paper-10932538. The frequency of IL-2- secreting cells and CD4/ CD8 ratio in BALF had a weak positive correlation. Paper-8842662. However, these leukemic cells proliferated in a IL-2 dose-dependent manner and expressed p55. Paper-5817545. Interleukin 2 regulates the activity of the lyn protein-tyrosine kinase in a B-cell line. Paper-7334362. Using chromatin immunoprecipitation, BACH2 was shown binding to the human IL-2 proximal promoter. Paper-13510945. Carboxy-terminal truncated STAT5 is induced by interleukin-2 and GM-CSF in human neutrophils. Paper-9236908. Mechanism of HDAC inhibitor FR235222- mediated IL-2 transcriptional repression in Jurkat cells. Paper-13413887. Schnurri-3 (KRC) interacts with c-Jun to regulate the IL-2 gene in T cells. Paper-10357587. Unlike CIS, SOCS-3 was rapidly tyrosine phosphorylated in response to IL-2. Paper-1908920. Normal or enhanced PHA- induced production of both IL-2 and IFN-gamma in vitro was detected. Paper-5408401. In contrast, IL-2 induced the higher NK activity and increased CD16 and CD56 Ag expression. Paper-6888188. CONCLUSIONS: SLC and IL-2 were produced by autocrine in DCs transfected with SLC and IL-2 genes. Paper-14051959. The production of both IL-1 and IL-2 was stimulated by a nanomolar concentration of CRF by itself. Paper-6768881. Hematopoietic effects of IL-2 are mediated by CD2/ LFA-3 receptor ligand interactions. Paper-5813448. Finally, proliferation induced by both IL-2- and IL-3 was significantly inhibited in the presence of SOCS-3. Paper-1908920. IL-2 up-regulates but IFN-gamma suppresses IL-8 expression in human monocytes. Paper-7656822. In addition, nine of the 15 SLE sera could inhibit the binding of 125I-labelled IL-2 to ATL-2 cells. Paper-5403041. The presence of IL-2- induced GM-CSF and M-CSF was also demonstrated by specific radioimmunoassays. Paper-6913638. On the other hand, MoAb CLB- CD28/1 induces response to IL-2 in thymocytes in the absence of accessory cells. Paper-21391. Down-modulation of IL-2- triggered JAK3- STAT5 signaling following CD4-ligand binding. Paper-1790854. The nature of the IL-2 transcriptional factors affected by VIP/ PACAP has not been elucidated. Paper-2146199. Furthermore, IL-2 and IL-12 synergistically induced IRF-1, whereas IFN-alpha and IL-12 did not. Paper-1883362. Although ILF bound constitutively to the IL-2 promoter, it was not detected as a component of the NFAT complex. Paper-952078. Inhibition of IFN-gamma production by IL-10 appears to be independent of the cytokine effect of IL-2 production. Paper-7242145. IL-5 production was observed in MNCs from lung cancer patients stimulated with IL-2, but not with IL-15. Paper-1555954. We then showed that AMPK inhibition reduced PMA/Io- induced IL-2 mRNA expression and IL-2 promoter activation. Paper-14714266. Phosphorylation at Ser647 of NF90 up-regulated IL-2 production in response to CD28 costimulation. Paper-12666769. Lymphokine- activated killer cells can discriminate CD34+ leukemia cells from normal hematopoietic progenitor cells. Paper-564536. Responding T cells were CD4-positive and produced interleukin-2 and interferon-gamma but no interleukin-4. Paper-1160835. Lymphokine- activated killer activity and natural killer activity in hepatocellular carcinoma patients were assessed. Paper-6246401. The eluate also displayed BCGF activity (tested on anti-mu- activated B-enriched cells) without detectable IL 2 activity. Paper-4867538. Both IL-4 and IL-2 induced upregulation of IL-4R on activated normal T cells but not on ATL cells. Paper-559331. Lymphokine- activated killer activity was impaired in hepatocellular carcinoma as compared to that in normal subjects. Paper-6246401. Interleukin-2 ( IL-2) rapidly activated Stat5 in fresh PBL, and Stat3 and Stat5 in preactivated PBL. Paper-209479. CD40 ligation inhibits IL-2 and SAC+IL-2 induced proliferation in chronic lymphocytic leukaemia cells. Paper-1066078. Interleukin 2 ( IL-2) induced a marked up-modulation and surface rearrangement of CD38 in all the patients studied. Paper-10000329. In contrast, IFN-gamma was significantly lower in RA (88 +/- 34 U/ml vs 209 +/- 32) with an associated deficit in IL 2. Paper-5429052. By contrast concentrations of PRL five- to tenfold the physiological levels inhibited the mitogenic response to IL2 and PHA. Paper-7468652. Th1- and Th2-type lymphokine-assisted induction and release of chemokine receptors from primary human trophoblast cells. Paper-8419016. A 44 kilodalton cell surface homodimer regulates interleukin 2 production by activated human T lymphocytes. Paper-5208821. Suppressor and cytolytic cell function in multiple sclerosis. Effects of cyclosporine A and interleukin 2. Paper-5148301. This resistance was associated with the enhanced ability of Melan-A/MART-1(27-35) 1L-specific T cells to release IL-2. Paper-9857838. We have determined that the loss of TRAF6 restores the ability of CD28(-/-) T cells to proliferate and produce IL-2. Paper-12666747. These results establish a crucial PI3K/ PKB- mediated link between the IL-2 teceptor and the cell cycle machinery. Paper-1240722. Stimulation of T cells via CD44 requires leukocyte- function- associated antigen interactions and interleukin-2 production. Paper-145008. Here we show that anti-CD28/ IL-2-primed Th2 cells expressed high levels of activated STAT6, but no cytokine mRNA. Paper-1376948. An anti- MUC1-antibody- interleukin-2 fusion protein that activates resting NK cells to lysis of MUC1-positive tumour cells. Paper-10034723. Dysregulation of B7.2 ( CD86) expression on monocytes of HIV-infected individuals is associated with altered production of IL-2. Paper-1916086. IL 2 induced proliferation not only in SAC-stimulated B cells but also in an anti-mu-stimulated B cell population. Paper-4884245. Vav and PKCtheta play an early and important role in the TCR/ CD28- induced stimulation of MAP kinases and activation of the IL-2 gene. Paper-2153625. These data suggest that IL-2 must stimulate both Erk2 activity and a further pathway(s) to trigger cell proliferation. Paper-99834. LT enhances the proliferation of activated B cells and augments B cell proliferation induced by IL-2. Paper-1392343. These results suggest that AMPK mediates IL-2 production by regulating NF-AT and AP-1activation during T cell stimulation. Paper-14714266. Here, using an inducible system, we demonstrate that Nef increases IL-2 secretion from T cells stimulated via CD3 or CD28. Paper-2086704. We demonstrate here that, in opposition with previous reports, recombinant IL2 also can up-regulate CD23 expression on B cells. Paper-6193974. Decreased 4-1BB expression on HIV-specific CD4+ T cells is associated with sustained viral replication and reduced IL-2 production. Paper-13885630. This suggested that Epo binding caused the activation of an IL-2 signal pathway mediated by the chimeric receptors. Paper-345059. Here we identify the cell cycle regulator E2F as an IL-2 target in T lymphocytes and PI3K as the critical signaling pathway. Paper-1240722. Reciprocal granzyme/perforin- mediated death of human regulatory and responder T cells is regulated by interleukin-2 ( IL-2). Paper-15105151. The augmented migratory capacity of IL-2- activated versus resting NK cells was associated with increased CCR2 transcript levels. Paper-1089285. The results show that the expression of phospho- STAT3 in spleen cell stimulated by IL-2 differ not from that in the unstimulated cell. Paper-12411506. Furthermore, the cells in the MS lesion expressed the interleukin 2 ( IL 2) receptor, as identified by the anti-TAC monoclonal antibody. Paper-5394810. Resting CD4+T cells must receive nonspecific costimulatory signals from APC to produce maximal amounts of IL-2 in response to TCR signaling. Paper-109112. T cells of donor HY were stimulated with the 3D6 antibody and subsequently expanded in recombinant interleukin 2-containing medium. Paper-5401208. Herein, we report that enzymatically active Raf-1 is physically associated with the IL-2 receptor beta chain ( p75) in T-cell blasts. Paper-66073. The CD7 Ag was found to be expressed at a significantly (p < 0.002) higher level on fresh NK cells than on IL-2-activated, NK cells. Paper-109114. The adaptor protein ALX acts downstream of CD28 to regulate the interleukin-2 ( IL-2) promoter during T cell activation. Paper-11474498. Moreover, transfection of primary T cells with c-Rel or p65 enhanced proliferation and production of IL-2 and IFN-gamma. Paper-10735541. The IL-2 toxin- mediated inhibition of protein synthesis in high affinity IL-2-R-positive murine and human T cell lines has been examined. Paper-6101311. AS101 inhibited the production of IL-2R, IL-5 and IL-10 and induced a significant increase in IL-2 levels in the mycosis fungoides PBMCs. Paper-9142981. Systemic lupus erythematosus serum IgG increases CREM binding to the IL-2 promoter and suppresses IL-2 production through CaMKIV. Paper-10776182. This indicates that IL-2 produced by fluA-specific T cells is involved in the T cell-dependent IFN-gamma response of NK cells to fluA. Paper-11433005. Reduction of serum CRP or IL-6 levels with thalidomide may enhance the responsiveness of renal cell carcinoma to IL-2. Paper-10239539. NF45 ( ILF2) and NF90 ( ILF3) regulate the IL-2 gene transcription via interaction with the antigen receptor response element. Paper-12140624. Cytokines IL-1 beta, TNF-alpha and IL-6 are preferentially stimulated by LPS whereas IL-2, IFN-gamma and GM-CSF are stimulated by PHA. Paper-7442876. We show that NKSF synergizes with IL-2 and phorbol diesters inducing the accumulation of IFN-gamma mRNA in PHA-activated T cell blasts. Paper-7208800. This report demonstrates the rapid activation of an IL-2 nuclear- activated factor that recognizes the same GAAA inverted repeat in the IRF-1 promoter. Paper-127002. In the performed heterodimer model the p55 and p75 chains form a non-covalently linked high affinity heterodimer in the absence of IL-2. Paper-7248468. IL-2 therapy affected serum tumor necrosis factor ( TNF), interferon gamma ( IFN gamma) and soluble IL-2 receptor (sIL-2r) levels. Paper-6908437. Mutations in the zinc finger domain of IKK gamma block the activation of NF-kappa B and the induction of IL-2 in stimulated T lymphocytes. Paper-12745903. Since IL-4 did not suppress IL-2 production, it would seem that the IL-2 producing subset in CD4+HLA-DR+ T cells is decreased in IDDM. Paper-128780. Binding of a radiolabeled IL2 preparation to the in vitro activated CML cells indicated the presence of low affinity receptors for IL2. Paper-5781563. Cross-linking CD28 was much more effective in inducing cyclin D3 expression and in down-regulating p27kip1 expression than addition of IL-2. Paper-1798547. Thus, CD18 mAb inhibited the apoptotic response to IL-2 deprivation, whereas mAb against other adhesion molecules (CD28, CD29, CD49d, CD80, CD86) did not. Paper-839555. Jak1 and Jak3 associated with IL-2R beta and gamma c, respectively; IL-2 induced Jak3-IL-2R beta and increased Jak3-gamma c associations. Paper-138530. Inhibition of MAPK signaling pathways using inhibitors of MEK, JNK or p38 abolished SIVagm3- induced IL-2 activation in a dose-dependent manner. Paper-10845752. Involvement of P-glycoprotein in the transmembrane transport of interleukin-2 ( IL-2), IL-4, and interferon-gamma in normal human T lymphocytes. Paper-661406. In addition, CRF augmented the production of IL-1 as induced by lipopolysaccharide and the production of IL-2 as induced by phytohemagglutinin. Paper-6768881. Interleukin-2 enhances the response of natural killer cells to interleukin-12 through up-regulation of the interleukin-12 receptor and STAT4. Paper-8499373. IL-2 up-regulated TLR4 surface expression on human peripheral blood monocytes, but did not change expression on human peripheral B cells. Paper-9193739. As expected, B-CLL lymphocytes proliferated with PMA, SAC and IL2 with a clear enhancement of the IL2- induced response by IFN alpha or IFN gamma. Paper-140874. When T cells were stimulated under weak stimulation conditions, pharmaceutical and molecular p38 inhibitors induced a dramatic increase of IL-2 production. Paper-11824683. Interleukin-2 ( IL-2) and other cytokines up-regulate the in vitro ET-1 release in guinea pig airway epithelial cells. Paper-143955. Combined use of interleukin 2 ( IL-2) and IL-4 promoted the internalization of CCR9 and therefore attenuated leukemia cell infiltration and metastasis. Paper-13864949. Mutagenesis of each of the two sequence elements required for ILF binding decreased IL-2 promoter activity when assayed in transfection assays. Paper-952078. Exogenous IL2 induces secretion of BCGF and IFN-gamma of the cloned cells, an observation which involves interaction of IL2 with IL2 receptors. Paper-5826599. Five short term TIL cell lines established in the presence of IL-2 expressed high level of IL-10, IL-4 and IFNgamma but not IL-2 mRNA. Paper-1466151. These results indicate that defective recruitment of NF-kappa B may underlie Nef's negative transcriptional effects on the HIV-1 and interleukin 2 promoters. Paper-7493766. Protein tyrosine phosphatase, non-receptor type 22 ( PTPN22) inhibits T-cell activation and interleukin-2 ( IL-2) production. Paper-14142160. Taken together these results suggest that TGF-beta may suppress immune responses by inhibiting the endogenous production of IL-2 and IL-6. Paper-6606587. Resistance of HER2/neu-overexpressing tumor targets to lymphokine-activated-killer-cell-mediated lysis: evidence for deficiency of binding and post-binding events. Paper-7781413. Interleukin-4 differentially regulates interleukin-2- mediated and CD2- mediated induction of human lymphokine-activated killer effectors. Paper-7216821. The addition of IL-1 consistently induced a low level of IL-2 production and strongly enhanced T-cell proliferation in the presence of IL-6. Paper-6559988. Suppression of IL-2- induced T cell proliferation and phosphorylation of STAT3 and STAT5 by tumor-derived TGF beta is reversed by IL-15. Paper-8995129. Incubation with the JNK inhibitor SP600125 inhibited the NKG2D expression induced by IL-2/ IL-18 in the TGF-beta treated human NK cell line. Paper-12357640. Gel shift assays of nuclear extracts immunodepleted of Ref-1 protein demonstrated that IL-2- induced AP-1 DNA binding is dependent on the presence of Ref-1. Paper-8612699. T4 cells reacted with mAb to class I MHC Ag or beta 2 microglobulin and cross- linked with GaMIg proliferated vigorously in the presence of IL-2 or PMA. Paper-5895832. Taken together with our previous observations, the present studies suggest that ICAM-1 is in proximity and interacts physically with the high-affinity IL-2 receptor. Paper-6507207. In fact, IFN-gamma, which is also a potent monocyte activator, not only failed to induce IL-8 expression but inhibited the stimulation of IL-8 by IL-2. Paper-7656822. However, co-culture experiments (IEL + LPMNC) have shown that IEL can enhance the PHA- induced synthesis of IL-2 and interferon-gamma, but not IL-10 by LPMNC. Paper-12793550. Nuclear export of NF90 to stabilize IL-2 mRNA is mediated by AKT-dependent phosphorylation at Ser647 in response to CD28 costimulation. Paper-12666769. The targeted expression of the human interleukin-2/interferon alpha2b fused gene in alpha-fetoprotein- expressing hepatocellular carcinoma cells. Paper-1792134. We also examined the effects of the culture supernatant of Con A- and IL-2- activated T-lymphocytes on CD11b expression on eosinophils in the present study. Paper-12793096. The activated PPARgamma physically associates with transcriptional factor NFAT regulating the IL-2 promoter, blocking NFAT DNA binding and transcriptional activity. Paper-2133901. These studies reveal a critical link between IL-2 mediated JAK- STAT5 signaling and the maintenance of Foxp3 expression in Treg of mice and humans. Paper-12333540. These results suggest that the accessory function of macrophages for IL 2- induced B cell activation is primarily on the induction of IL 2R on B lymphocytes. Paper-5208822. Endogenous IL-15 sustains recruitment of IL-2Rbeta and common gamma and IL-2- mediated chemokine production in normal and inflamed human gingival fibroblasts. Paper-10660634. We also demonstrate that DUSP5- expressing mature T cells exhibit decreased IL-2-dependent proliferation and defective IL-2-mediated induction of genes. Paper-12832406. Addition of IL-2 or IL-15 to short-term in vitro cultures of either PBMCs or CD4+ T cells had little effect on IL-2, IL-4, or IFN-gamma production. Paper-379022. It has been noted that response to IL-2 and prognosis may be adversely affected by elevated serum levels of C-reactive protein ( CRP) or interleukin-6 ( IL-6). Paper-10239539. Interferon-alpha and interleukin 2 synergistically enhance basic fibroblast growth factor synthesis and induce release, promoting endothelial cell growth. Paper-7880934. Exogenous IL-10 reversed the inhibitory effect of a high dose of IL-2 on the killing activity by reducing TGF-beta 1 mRNA expression in T cells and its production. Paper-1299619. Human immunodeficiency virus-1 envelope glycoproteins and anti-CD4 antibodies inhibit interleukin-2- induced Jak/STAT signalling in human CD4 T lymphocytes. Paper-9876970. Introduction of inhibitory cells ( Leu8) into a population that actively expressed IL-2 and IFN-gamma mRNA resulted in an immediate cessation of gene expression. Paper-205481. When PHA- activated T lymphoblasts were cultured for 16 days with IL-2, IFN-gamma R alpha expression increased, whereas that of the beta-chain remained barely detectable. Paper-715408. Consistent with this, in TRAF6-deficient T cells, TGF-beta more effectively down-regulates interleukin-2 ( IL-2), a known inhibitor of Th17 differentiation. Paper-15156002. A comparable down-modulation of IL-2 release could also be induced by the MART-1-derived peptide 32-40, previously identified in one of the two anergizing fractions. Paper-9857838. We have previously demonstrated that IL-9 induction in human T cells stimulated with PMA and anti-CD3 Ab is mediated by IL-2, as it was blocked by anti-IL-2R Ab. Paper-174853. The cells from these patients that respond to exogenous IL-2 are CD56+ natural killer cells expressing intermediate-affinity IL-2 receptor betagamma(c) complexes. Paper-1473851. Up-modulation of a 32S-methionine-labelled 27,000 MW protein was detected in the lysates and supernatants of IL-2- stimulated PBMC immunoprecipitated with an anti- PRL antiserum. Paper-866285. In contrast, UCHL-1- cells seem to mediate the inhibition of Ag-driven IL-2 production by nonadherent cells but not mitogen-stimulated IL-2 secretion by nonadherent cells. Paper-6916805. However, stimulation in vitro triggered these cells to express Foxp3 as well as CD25, and the addition of interleukin-2 possibly enhanced the expression of Foxp3. Paper-12975393. Potential role of phospholipase D2 in increasing interleukin-2 production by T-lymphocytes through activation of mitogen- activated protein kinases ERK1/ ERK2. Paper-14321459. Janus kinase 3 regulates interleukin 2- induced mucosal wound repair through tyrosine phosphorylation of villin. Paper-12523112. The combination of SA, anti-CD40, and IL-4 induced one tenth of the total Ig production that was stimulated by SA and IL-2, with a different distribution of Ig H chain isotypes. Paper-7583340. In both MS groups IL-2 receptor expression on PBMC stimulated with MBP appeared higher than in control groups, but these differences were not statistically significant. Paper-6114254. CONCLUSION: Enhanced IL-2 production in stimulated T cells expressing HIV-Nef is associated with increased activation of PI3K-dependent signalling pathways. Paper-8748732. The Th1 cytokines were expressed at greater levels than the Th2 cytokines, with strong CASA significantly associated with an increased inducible level of IL-2 production (P=0.05). Paper-9396531. Knockdown experiments of BACH2 by transient transfection of UCB CD4(+) T cells with BACH2 siRNA resulted in significant reductions in stimulated IL-2 production. Paper-13510945. To investigate the roles of PKD2, wild-type (WT) and constitutively active (CA) PKD2 were expressed in Jurkat cells together with IL-2 promoter-driven reporter gene. Paper-12331974. Interleukin (IL)-15 and IL-2 reciprocally regulate expression of the chemokine receptor CX3CR1 through selective NFAT1- and NFAT2-dependent mechanisms. Paper-10630708. Direct recognition of SLA- and HLA-like class II antigens on porcine endothelium by human T cells results in T cell activation and release of interleukin-2. Paper-421727. In clones stably overexpressing hIRAK a weak constitutive activation of NFkappaB correlated with a low basal IL-2 production which was enhanced in an IL-1-dependent manner. Paper-1648123. This selectivity may contribute to regulation of the levels of IL-2 induced by LFA-3 and B7-1 costimulation and favor autocrine and paracrine T-cell responses, respectively. Paper-903729. Recombinant IL-2 induced increased p24 in cultures from 8 of 13 symptomatic subjects, but rIL-12 did only in cell lines from 5 symptomatic subjects and then only marginally. Paper-655100. These results indicate that IL-2 activation of human NK cells induces significantly higher levels of lytic activity than does conventional ADCC involving IgG and FcRIII. Paper-1702433. In this research, we studied the expression and function of CCR3 induced by interleukin-2 ( IL-2) and interleukin-4 ( IL-4) on human germinal centre (GC) B cells. Paper-11094863. Triggering of Fc epsilon RII/ CD23 resulted in the enhanced expression of IL-2R/p55(Tac), whereas IL-2 enhanced the expression of Fc epsilon RII/ CD23 in some systems. Paper-5463. The age-associated changes of the expression of IL-2 binding molecules p55/Tac(alpha chain) and p70/75(beta chain) were examined after phytohemagglutinin (PHA) stimulation. Paper-6011904. Therefore, up-regulation of TIMP-1 expression by IL-2 likely contributed to the additive effect of IL-2 and TIMP-1 in reducing metastatic disease in the animal model. Paper-9223664. This BCGF- induced proliferation was not influenced by IL 2 or interferon-gamma ( IFN-gamma), because both recombinant IL 2 and IFN-gamma failed to induce proliferation. Paper-5482808. Activation of antigen-induced lymphocyte proliferation by interleukin-15 without the mitogenic effect of interleukin-2 that may induce human immunodeficiency virus-1 expression. Paper-609343. Granulocyte colony stimulation factor ( G-CSF) suppresses interleukin (IL)-12 and/or IL-2 induced interferon (IFN)-gamma production and cytotoxicity of decidual mononuclear cells. Paper-10004352. Different sensitivity to interleukin 4 of interleukin 2- and interferon alpha- induced CD69 antigen expression in human resting NK cells and CD3+, CD4-, CD8- lymphocytes. Paper-7265661. In addition, our results indicate that the stimulatory effect of IL-2 can be down-regulated by IL-4 with respect to both LAK activity and granzyme B and perforin gene expression. Paper-11755426. The addition of gamma-IFN together with IL 2 induced IgM and IgG secretion in SAC-stimulated B cells that was comparable with that induced by a conventional T cell factor(s). Paper-4884245. Isolated CD4(+)CD25(+) T cells are susceptible to apoptosis that is associated with low Bcl-2 expression, but this death can be prevented by IL-2 or fibroblast- secreted IFN-beta. Paper-8726440. After CD16 cross- linking and stimulation with IL-2 or IL-15 NK cells produced CC-chemokines to levels comparable to those produced by anti-CD3-stimulated CD8(+) T cells. Paper-1485160. Purified human NK cells activated in the presence of IL2 for 24 hr upregulated the expression of the CD11c (p150.95) and CD11a antigen but not other cellular adhesion molecules (CAM). Paper-7194415. Activation of phospholipase C-gamma 1 through transfected platelet-derived growth factor receptor enhances interleukin 2 production upon antigen stimulation in a T-cell line. Paper-110063. Finally, these complexes on activated monocytes present IL-15 in trans to target cells such as CD8(+) T cells that express only IL-2/15Rbeta and gammac upon cell-cell interaction. Paper-9586328. Interferon-alpha gene transfer downregulated c-myc, EGF-R, and type IV collagenase mRNA expression, whereas only the higher producers of IL-2 downregulated TGF-beta mRNA expression. Paper-131847. Ca(2+)/calmodulin-dependent kinase IV (CaMKIV) was found to be increased in the nucleus of SLE T cells and to be involved in the overexpression of CREM and its binding to the IL-2 promoter. Paper-10776182. We report here that, upon stimulation by autologous melanoma cells, all TIL clones secreted TNF but only a few of them produced significant amounts of IL-2, IL-4 or IFN-gamma. Paper-132326. In conclusion, the results obtained show that leptin modulates CD4(+) and CD8(+) cell activation towards a T helper 1 (Th1) phenotype by stimulating the synthesis of IL-2 and IFN-gamma. Paper-13230404. IFN-gamma is found to double both the number of positive cells and the number of binding sites, whereas IL 2 has no influence on the IL 2 receptor expression on monocytes. Paper-5208066. Signaling normal human T-cells: synergism between CD2 antigen and CD3/ T cell receptor alpha beta complex in the elicitation of IL-2 and IL-2 receptor gene expression. Paper-7158299. In addition, IL-2 stimulated the NK cells to release soluble FasL in a time-dependent manner, whereas membrane FasL did not seem to increase in a similar manner. Paper-1918712. The loss of ASGPR binding activity mediated by IL-2 was reversible up to 4 hours of exposure and accompanied by the selective phosphorylation of the cell-surface receptor. Paper-114378. A high percentage of IFN-gamma- and IL-2- producing cells was observed among the PB T cells in both the RA patients and normal controls and among the SF T cells in RA patients. Paper-9529129. GM-CSF and IFN-gamma release from activated T cells increased four- to fivefold in response to 1 nM IL-2 and IL-2 augmented both GM-CSF and IFN-gamma mRNA. Paper-6918694. Furthermore, the data argue for a predominant activation of an IL-2- and sIL-2R- producing but not IL-4-producing T-helper (Th) lymphocyte subpopulation, Th1/ CD4 + CD45R + cells. Paper-6918446. DCs infected with HSV-1 showed enhanced surface expression of the costimulatory molecule CD252 ( CD134L) compared with Listeria-infected DC and induced enhanced secretion of IL-2. Paper-13821136. The major differences between CD28 and ICOS are differences in expression of both receptors and ligands, and the fact that CD28 induces IL-2 production, whereas ICOS does not. Paper-12030403. Exogenous IL-2 and/or IFN-alpha treatment of a IFN-alpha-resistant RCC enhanced both HLA class I antigen and ICAM-1 expression and suppressed CD44 expression, but had no effect on tumor growth rate. Paper-131847. This investigation focuses on the IL-2 induced regulation of Sgk1 and describes a role of the IL-2 receptor and Sgk1 in the regulation of epithelial tumor cell death and survival. Paper-13337059. MMP II-specific bulk T cell lines were established from leprosy patients to determine major T cell epitopes in MMP II and to evaluate lymphokine production induced by MMP II. Paper-8888660. CONCLUSION: Weak evidence of linkage of RA to IL5R, IFN gamma, and IL2 has been detected in clinical subsets of sibling pairs suggesting that RA is a genetically heterogeneous disease. Paper-1580859. In the present study we have examined the potential contribution of IL-2/IL-2R interactions in CD3- mediated responses by T lymphocytes from patients with systemic lupus erythematosus ( SLE). Paper-107886. We also detected an expansion of TCR1+ cells in IL-2- stimulated PBL employing the pan-gamma/delta marker TCR delta 1; however, in contrast to solid organs, these TCR1+ cells were delta TCS1 negative. Paper-131914. Pretreatment with anti-IL-15 neutralizing mAb for 24 h completely inhibited the production of MCP-1 induced by IL-2 and IL-15 and IL-2-induced phosphorylation of Jak 1 and 3 in HGF. Paper-10660634. This cooperation between ICOS and IL-2 signaling was explored further by showing that the minimum level of IL-2 produced by ICOS costimulation was required for T cell proliferation. Paper-8807724. These findings suggest that crosslinking CD7 and FcRmu inhibits T-cell activation and proliferation by a calcium-dependent mechanism that inhibits IL-2 production and/or utilization. Paper-7327476. The IL-2 producing ability of lymph node mononuclear cells was found to be significantly higher than that of peripheral blood mononuclear cells from both healthy donors and NHL patients. Paper-7868834. Accordingly, induction of IL-2 secretion upon receptor cross- linking by membrane- bound antigen requires CD28/B7 costimulation whereas IFN-gamma secretion and cell proliferation does not. Paper-8719763. Studies were conducted to investigate further IL-2- induced maturation of oligodendrocytes through its effect on the regulation of the myelin basic protein ( MBP) gene. Paper-5623007. Activation via the CD3 and CD16 pathway mediates interleukin-2-dependent autocrine proliferation of granular lymphocytes in patients with granular lymphocyte proliferative disorders. Paper-6923126. In conclusion, our results indicate that RA, via RAR, stimulates IL-2- induced signaling in a JAK-dependent manner to enhance cyclin D3 expression and thereby promote T cell proliferation. Paper-12184897. Thus, HCS enhances the lectin- induced expression of IL2-receptors as evidenced by both increased responsiveness to IL2 and increased capacity to absorb IL2 of HCS-treated thymocytes. Paper-5135054. The fluA-induced IFN-gamma production of NK cells was suppressed by anti-IL-2 Ab, while recombinant IL-2 replaced the helper function of T cells for IFN-gamma production by NK cells. Paper-11433005. The effects of three classes of recombinant interferons ( IFN-alpha A, IFN-beta, and IFN-gamma) on maximal induction of lymphokine (IL-2)- activated killer ( LAK) activity were studied. Paper-5827181. Strong CASA was therefore associated with rapidly replicating CD8+ T cells of the phenotype CD8+CD28+Ki67+ that expressed greater levels of IL-2 and the ligands RANTES and I-309. Paper-9396531. Disruption of the lymphokine network (anti-interleukin-10 antibody) and the function of adhesion-costimulatory molecules (CTLA-4-immunoglobulin) were shown to be therapeutically significant in murine SLE. Paper-438960. In man, IL2 appears to play a central role in regulating B cell activation, proliferation and differentiation, whereas IL4 plays a regulatory role by inhibiting initial B cell activation. Paper-5864639. Since CD95 ligand ( CD95L) is expressed on interleukin-2 (IL-2)-activated T cells, we investigated the involvement of CD95- CD95L pathway in T cell-mediated cytotoxicity against AML cells. Paper-863038. Decreased CCR5 surface expression was not secondary to transcriptional inhibition, given that CCR5 mRNA was enhanced in cells cultured in IL-12/ IL-2 compared with those cultured in IL-2 only. Paper-2038719. These findings indicate that the loss of 4-1BB on HIV-specific CD4+ T cells is associated with viral replication and that it may contribute to reduced IL-2 production observed during chronic infection. Paper-13885630. Micronutrients alone increased the ratio of CD4(+) to CD8(+) but not of CD4(+)CD45RA(+) to CD4(+)CD45RO(+), increased IFN-gamma but had no effect on IL-2 or IL-10, and increased sIL-1ra but not sTNF-R1. Paper-13026824. Through expression of high levels of IL-12 receptors and STAT4, IL-2-primed NK cells show enhanced functional responses to IL-12 as measured by IFN-gamma production and the killing of target cells. Paper-8499373. T4 cell proliferation in the presence of IL-2 and PMA could also be induced by reacting the cells with specific mAb to polymorphic determinants on class I MHC molecules and cross-linking with GaMIg. Paper-5895832. Acquired erythropoietin responsiveness of interleukin-2-dependent T lymphocytes retrovirally transduced with genes encoding chimeric erythropoietin/ interleukin-2 receptors. Paper-345059. In an earlier study, we established CD26-transfected Jurkat T-cell lines and demonstrated that monoclonal antibody-mediated crosslinking of CD26 and CD3 induced interleukin 2 ( IL-2) production. Paper-91664. In the presence of IL-2, recombinant APO2L/TRAIL or cytotoxic anti-Fas monoclonal antibodies induce rather inhibition of IL-2-dependent growth and not cell death on normal human T cell blasts. Paper-10761332. Moreover, JAK3 became tyrosine phosphorylated in response to IL-2, IL-4, and IL-7 but not response to IFN-gamma or granulocyte/macrophage colony-stimulating factor. Paper-189816. In addition, it was demonstrated that cross-linking class I MHC molecules by culturing T4 cells with immobilized mAb to class I MHC Ag induced T4 cell proliferation in the presence of IL-2. Paper-5895832. T-cell receptor complex phosphorylation and activation of the interleukin-2 pivotal transcriptional complex protein CREB were also simultaneously depressed as c-Cbl and SHP-1 were elevated. Paper-13170781. Studies on the inhibitory activity of transforming growth factor-beta demonstrated that this cytokine differs from IFN-gamma because it inhibited both IL-1- and IL-2- induced IL-6 expression. Paper-7237043. IFN-alpha A and IFN-beta also inhibited the proliferative responses of lymphocytes to IL-2 stimulation, and the expression of IL-2 receptors on their surface, whereas IFN-gamma did not. Paper-5827181. Results showed that the peak of IL2 production occurred on the second day of culture and was significantly suppressed by HSF while IL1 production was not affected during the seven day culture period. Paper-6013131. The modulated expression of KIR by IL-2 and TGF-beta can be associated with the changed NK-cytotoxic target-discriminating ability of NK cells upon their exposure to IL-2 and TGF-beta. Paper-10478996. Using chromatin immunoprecipitation, we have demonstrated that Foxp3 binds to the endogenous IL-2 and IFNgamma loci in T cells, but only after T cell receptor stimulation. Paper-12332183. IL-13 does not significantly inhibit the IL-2- induced T lymphocyte production of IFN-gamma, RANTES, MIP-1 alpha or MIP-1 beta, nor that of perforin mRNA, as does IL-4. Paper-1152452. Expression of WT- PKD2 enhanced IL-2 promoter activity upon stimulation with anti-CD3 mAb, while expression of CA- PKD2 inhibited IL-2 promoter activity and induced cell death. Paper-12331974. Thalidomide reduces serum C-reactive protein and interleukin-6 and induces response to IL-2 in a fraction of metastatic renal cell cancer patients who failed IL-2-based therapy. Paper-10239539. Addition of the specific MAPK inhibitor UO126 to JAR cells prior to the addition of activated PBMC to the cultures did not abolish the capacity of JAR cells to inhibit IL-2 mRNA expression in PBMC. Paper-10173312. Interleukin-2 inhibits glucocorticoid receptor transcriptional activity through a mechanism involving STAT5 (signal transducer and activator of transcription 5) but not AP-1. Paper-8848626. The present study demonstrates a novel pathway in intestinal enterocytes in which IL-2 enhances intestinal wound repair through mechanisms involving Jak3 and its interactions with villin. Paper-12523112. Here, we report that PKCtheta function was selectively required in a Vav signaling pathway that mediates the TCR/ CD28- induced activation of JNK and the IL-2 gene and the upregulation of CD69 expression. Paper-2153625. CD28 and CTLA-4 mRNA were detected in efferent lymph and afferent lymph populations containing CD4 and CD8 T cells stimulated with Con A and IL-2 or with Con A alone, respectively. Paper-1201793. Using freshly isolated peripheral blood mononuclear cells, we demonstrate that p17 was able to enhance levels of tumor necrosis factor alpha and IFN-gamma released from cells stimulated by IL-2. Paper-9166967. Expression of gp39 by activated T cells from patients with common variable immunodeficiency (CVI) is low in approximately half of the patients and is associated with depressed expression of IL-2. Paper-169177. We conclude that the MAP kinase signal transduction pathway consisting of Raf-1, MEK1, and ERK1 and ERK2 functions in the stimulation IL-2 gene transcription in activated T lymphocytes. Paper-474124. The same effects of CD40L were observed when B cells were stimulated by a combination of IL-2 and IL-4 and this inhibition could not be abrogated by increasing the amounts of IL-4. Paper-8478526. Between patients with MS and AM there was no difference regarding frequency of IL-2 secreting cells in response to any of the tested antigens except MAG to which the response was higher in MS patients. Paper-7759304. B7 selectively increased T cell proliferation and IL-2 secretion without affecting IFN-gamma production, whereas IL-12 increased both IL-2 and IFN-gamma production. Paper-8484651. Here we show that priming of CD4 T cells selectively enhances IL-4 expression relative to IL-2 expression by a transcriptional mechanism involving nuclear factor of activated T cells ( NFAT) proteins. Paper-1709715. However, after incubating LPC first and washing it from the cells, both lectins were able to stimulate secretion of higher levels of bioavailable IL2, but again, less IL2 was produced with PHA than with ConA. Paper-7125110. These results suggest that IL-18 activates NF-kappaB and it is important for enhancement of IL-2 gene expression by Th1 cells stimulated with IL-18. Paper-1051627. RESULTS: Both IL-2-gene- and IFN-alpha-gene- modified R11 exhibited enhanced expression of ICAM-1, suppression of CD44, and decreased binding affinity to ECM components, when compared with the R11-control vector. Paper-131847. The level of IFN-alpha- induced LAK activity was significantly greater than that induced by IFN-gamma, although IL-2- induced LAK activity was considerably greater than IFN-alpha-induced LAK cytotoxicity. Paper-6164266. HIV-1 Tat inhibits IL-2 gene transcription through qualitative and quantitative alterations of the cooperative Rel/ AP1 complex bound to the CD28RE/ AP1 composite element of the IL-2 promoter. Paper-8767130. In addition to the inhibitory effect, IL2 appeared to limit the stimulating effect on granulopoiesis and erythropoiesis of myeloid growth factors (GF) such as combination of IL3, GM-CSF and EPO. Paper-127781. Immunomodulatory drugs (IMiDs) increase the production of IL-2 from stimulated T cells by increasing PKC-theta activation and enhancing the DNA- binding activity of AP-1 but not NF-kappaB, OCT-1, or NF-AT. Paper-11248933. Preincubation of monocytes with mAbs directed to selected epitopes on CD14 blocked the binding of IL-2 to the cell surface, providing a possible explanation for the inhibition of IL-2-triggered responses. Paper-1163190. In fact, co-treatment of monocytes with IL-2 and IL-4 increased the expression of IL-2R gamma chain above the levels induced by IL-2 alone, whereas it did not significantly affect the expression of IL-2R beta chain. Paper-314060. Increased GC therapy of both groups taken together was associated with significant reductions in the percentages of PBMC expressing mRNA encoding IL-5, IL-4 and IL-2 and an increase in those expressing IFN-gamma mRNA. Paper-992439. The proliferation of CTLs stimulated by immobilised anti-CD3 monoclonal antibody and interleukin 2 ( IL-2) was enhanced three or four times by immobilised FN. whereas soluble FN did not alter the DNA synthesis of CTLs. Paper-779642. These results suggest that stimulation with a combination of IL-12- and CD80- modified tumor cells and subsequent expansion with IL-2 may efficiently generate tumor-specific CTLs from autologous peripheral blood lymphocytes. Paper-1419326. Stimulation of U937/ CD14 cells with IL-2 up-regulated the constitutive levels of IL-8 mRNA, whereas no change in IL-8 mRNA basal expression was observed in control cells transfected with the vector alone (U937/Neo). Paper-1163190. The significance of an increase in soluble interleukin-2 receptor level in colorectal cancer and its biological regulating role in the physiological switching of the immune response cytokine network from TH1 to TH2 and back. Paper-1297964. The immunosuppressive activity of a JEG-3 choriocarcinoma-derived factor in human IL-2-dependent T cell responses has been studied, together with its effect on IL-2-independent T cell responses induced by 10 nM TPA. Paper-6962670. Expression of MEK1-interfering mutants inhibited the stimulation of IL-2 promoter-driven transcription and blocked the ability of constitutively active Ras and Raf-1 to costimulate NF-AT activity with a calcium ionophore. Paper-474124. Alveolar macrophages from patients with arcoidosis, TB, and HB express the costimulatory molecule CD80 on their surface and anti-CD80 antibodies inhibited the IL-2 release of Jurkat cells in this system to 59 +/- 27%. Paper-963123. These data demonstrate that, in human monocytes, both IL-1 and IL-2 stimulate IL-6 expression by independent mechanisms that can be dissociated by the susceptibility to the inhibitory effect of IFN-gamma. Paper-7237043. To investigate the role of HSF- induced IL2 suppression in the pokeweed mitogen (PWM) antibody synthesis assay, the time course of IgG, IgM, IL1, and IL2 production of PWM stimulated PBMC cultures was examined. Paper-6013131. In this report, we have investigated the kinetics of IL-2 binding to the alpha (p55) and beta ( p70) IL-2 binding proteins and compared these properties with ligand binding to the high-affinity IL-2-R. Paper-5787538. In response to MAG, MOG and acetylcholine receptor (AChR) the frequencies of IL-2 secreting cells were higher in patients with MS than TH, while there were no differences between AM and TH to any of the tested antigens. Paper-7759304. In contrast to the marked changes of TRIM22 during activation of crude T lymphocytes, in isolated subpopulations, TRIM22 expression was not significantly affected in spite of IL-2-induced or CD3/CD2/CD28-induced activation. Paper-12588596. CIS1 is induced by interleukin-2 ( IL-2), IL-3, GM-CSF, and erythropoietin ( EPO), but not by IL-6, granulocyte colony-stimulating factor ( G-CSF), or stem cell factor. Paper-8295694. We previously have generated a single-chain T cell receptor-cytokine fusion protein (264scTCR/ IL-2) comprising interleukin-2 genetically linked to a soluble HLA-A2.1-restricted TCR recognizing a peptide of human p53 protein. Paper-12239900. The molar potency of IL-2 and the inhibitory activity of each of the above antibodies suggest that high affinity heterodimeric IL-2 receptor complexes mediated the migration responses of eosinophils to IL-2. Paper-6898151. In addition, while HLA-G- expressing transfectants of LCL.721.221 cells are protected from lymphokine-activated killer lysis, extravillous cytotrophoblast cells and HLA-G-expressing choriocarcinoma cells (CC) are not. Paper-1860532. Furthermore, the transcriptional activity of interleukin-2 ( IL-2) was enhanced in DOCK2- expressing Jurkat cells and the dominant negative form of Rac2 suppressed its elevated IL-2 promoter activity. Paper-9219334. Upon TLR-induced maturation, all DC became potent stimulators of CD4(+)CD25(-) T cells, whereas only TLR7- or TLR9-matured pDC induced strong proliferation of CD4(+)CD25(+)Foxp3(+) T cells in the absence of exogenous IL-2. Paper-12788874. Our results indicate that both MKK6 to p38 and MKK7 to SAPK/JNK signaling pathways are activated in a cyclosporin A-sensitive manner and contribute to IL-2 gene expression in T lymphocytes. Paper-1439812. In the presence of the 33B3.1 mAb, the interaction of TU27 with IL-2 resembled the one observed on YT-2C2 cells, suggesting that 33B3.1 is able to inhibit the IL-2- induced association of p55 and p75. Paper-6867124. However, IL-2 promoted cell cycle progression in cells bearing the truncated huIL-2R beta with percentages of viable cells in the G0/ G1, S, and G2/ M phases similar to cells expressing the wild-type huIL-2R beta. Paper-1376962. Interleukin 2 ( IL-2) stimulated activation of the 42-kD extracellular signal-regulated kinase 2 ( Erk2) in murine IL-3-dependent cells, expressing either high or intermediate affinity IL-2 receptors. Paper-99834. TCR-activated primary T cells from healthy donors treated with c-Rel antisense oligonucleotides produced lower levels of IL-2 and IFN-gamma and proliferated less efficiently than the corresponding control T cells. Paper-10735541. The effect of IL-4 upon IL-2- induced LAK cell expansion is thus very different on PBMC pre- activated in vivo by alpha IFN + IL-2 therapy than on PBMC pre-treated in vitro with IL-2.(ABSTRACT TRUNCATED AT 250 WORDS) Paper-6829684. In this study, HIV-1 gp41 was a potent modulator of cytokine production by PBMC, in particular by increasing IL-10 secretion from normal monocytes/ macrophages and consequently down-regulating IL-2 and IFN-gamma. Paper-1377045. The large amounts of IL-2 produced by B7 costimulation indicate a paracrine function of the B7/ CD28 pathway, whereas the LFA-3/ CD2 pathway provides strong adhesion and may facilitate autocrine T cell expansion. Paper-131062. We have shown that the sera of lung cancer patients affect the response of ConA- stimulated normal peripheral blood mononuclear cells by decreasing the expression of IL-2Ralpha and inhibiting the release of IL-1beta and IL-2. Paper-10556040. Whereas among CD45RA+ CD4+ T-cells both CD31+ and CD31- subsets produce interleukin-2 ( IL-2) upon PMA/ ionomycin stimulation, only the CD31- subpopulation is able to produce IFN-gamma. Paper-1169376. PRLIF and IL-2 nuclear- activated factor are newly identified factors that appear to serve fundamental roles in the signal transduction pathways of PRL and IL-2, respectively, leading to the transcriptional regulation of responsive genes. Paper-127002. In vivo IL-2 also dramatically modified the bone marrow T-cell subsets via the increase of CD3+ cells expressing the CD45RO 'memory' marker (six out of the eight tested patients) or CD54 (seven out of the eight tested patients). Paper-126207. After stimulation with a combination of anti- CD26 and anti-CD3 antibodies, wild-type CD26 (DPPIV+)-transfected Jurkat cells produced substantially more IL-2 than did mutant CD26 ( DPPIV-) or CD26- control transfectants. Paper-91664. However, contrary to FK506, which blocks IL2 synthesis, we observed that FAP48- FKBP complexes increase IL2 production, thus revealing a previously uncharacterized aspect of the immunosuppressive mechanism of FK506. Paper-9879194. The cells infected with the bFGF- expressing adenovirus containing the IL-2 signal sequence showed 2- to 10-fold higher levels of secretion levels than cells infected with the native bFGF-expressing adenovirus alone. Paper-8519478. Therapy of recurrent high grade gliomas with surgery, and autologous mitogen activated IL-2 stimulated killer ( MAK) lymphocytes: I. Enhancement of MAK lytic activity and cytokine production by PHA and clinical use of PHA. Paper-7792143. This study was undertaken to determine if prolonged daily subcutaneous administration of ultra low dose IL-2 could influence the constitutive endogenous production of a type 1 ( IFN-gamma) cytokine in patients with AIDS or AIDS-associated malignancies. Paper-1380245. The transcription factor, Nuclear Factor of Activated T cells ( NFAT) is a major target for p21ras and calcium signalling pathways in the IL-2 gene and is induced by p21ras signals acting in synergy with calcium/calcineurin signals. Paper-654748. These data suggest that engagement of LFA-1 can provide sufficient costimulatory signals to induce T cell activation and IL-2 gene expression, but cannot protect against anergy induction or provide for T cell survival. Paper-1376932. Sequenom Quantiative Gene Expression (QGE) (SanDiego, CA) measures confirmed IL2, IL4 and IFNgamma up-regulation in Tempus purified RNA from PHA stimulated cells while only IL2 was up-regulated using PAXgene purified (p < 0.05). Paper-13057970. First, we showed that hCD152- hCD59 expression prevents the binding of murine CD28Ig to pCD86 on porcine aortic endothelial cells (PAEC) and dramatically reduces IL-2 secretion by Con A-stimulated mouse splenocytes in coculture. Paper-10540694. PURPOSE: To examine interleukin-7 ( IL7)- and interleukin-2 (IL2)- induced proliferation of Sézary lymphoma cells and to consider if an autocrine or paracrine growth-stimulatory circuit involving IL7 exists in the Sézary syndrome (SS). Paper-113074. TGF-beta 1 had no effect on basal release of CRF, nor on the CRF- release induced by IL-2, but selectively blocked the acetylcholine-induced release in both amygdala and hypothalamus. Paper-1071149. Costimulation through both CD82 and CD3 induced up-regulation of both IL-2 and IFN-gamma mRNA synthesis (but not of IL-4) and an increased expression of HLA class I molecules at the cell surface, which was inhibited by anti-IFN-gamma Ab. Paper-278607. T lymphocytes from thyroid infiltrate and peripheral blood (PB) of four patients with Hashimoto's thyroiditis ( HT) were analysed at clonal level for their ability to secrete interleukin 2 ( IL-2) and gamma-interferon (gamma-IFN). Paper-5787252. The outgrowth of simian gamma delta T cells in response to Daudi cells is similar to that in humans, but the exposure to IL-2 stimulates preferentially the simian V delta 1 subset rather than the V gamma 9/V delta 2 subset as found in humans. Paper-412830. However, the CTL stimulated by either the native MUC1-mtr1 or (T3N) MUC1-mtr1 showed 5-10 times greater cytotoxicity of a breast cancer cell line that expresses MUC1 compared to CTL stimulated by either anti-CD3 + IL-2 or IL-2 alone. Paper-10576602. IL-2 activates mitogen-activated protein kinase ( MAPK), phosphatidylinositol 3-kinase, and signal transducer and activator of transcription (STAT) pathways and modulates expression of target genes. Paper-12832406. Although all NFAT family proteins contain a highly conserved DNA- binding domain and also bind cooperatively with AP-1 proteins to the interleukin-2 ( IL-2) promoter NFAT site, each member shows characteristic site preferences to other promoters. Paper-9410224. Furthermore, its negative effects on NFAT1 protein and downstream interleukin-2 ( IL-2) transcription are reversed through antisense blocking in UCB and can be replicated via exogenous transfection of precursor miR-184 into AB CD4+ T cells. Paper-13856998. A T-cell zone comprising CD4-positive helper T cells, CD8-positive suppressor/cytotoxic T cells and a few CD25-positive activated T cells expressing interleukin-2 receptor was seen at the periphery of the nodules. Paper-7705490. The possibility that IL 7 mediates its growth stimulation by the IL2 pathway was excluded by the incapacity of anti-IL2 or anti-Tac monoclonal antibody, in concentrations which blocked IL2-dependent proliferation, to inhibit IL 7-dependent growth. Paper-6501677. We have shown that treatment with interleukin-2 ( IL-2) or interferon-alpha (IFN alpha) may induce depressive symptoms and activation of the cytokine network and that IL-2 treatment may diminish serum dipeptidyl pepdidase IV ( DPP IV) activity. Paper-9004224. These results suggest that STPM inhibit lymphocyte proliferation by affecting one or several events occurring in the synthesis and/or expression of IL-2R P55 by a mechanism which is at least partially independent of its inhibitory effect on IL-2 secretion. Paper-6914566. Although the lymphocytes showed LAK activity against class I expressing targets following IL-2, IL-12 and IL-15 stimulation for 3 days, neither NK nor LAK activity against targets lacking class I molecules was induced. Paper-1758214. Examination of transcription factor activation and IL-2 gene expression in Jurkat T cells revealed that sarcoid but not normal ELF activated AP1 and NF-kappaB, induced IL-2 gene transcription, and up-regulated IL-2 protein production. Paper-8624105. Our data indicate that CD40 and CD80 molecules might play a preferential role in the induction of cytotoxic function but not in the interferon-gamma(IFN-gamma) production by human IL-2-activated NK effectors in the presence of autologous and allogeneic DCs. Paper-10404306. The specificity of the hrlL-2-induced response was defined in experiments in which mitogenicity of this T cell growth-promoting lymphokine was completely abrogated by blocking the T cell membrane receptor for IL-2 with the anti-Tac monoclonal antibody. Paper-4879644. In particular it appears that IL-6 acts as a costimulatory signal with IL-2 in generating CTL and that IL-6 functions in part by acting in synergy with IL-2 to induce PFP, a major lytic protein involved in lymphocyte cytotoxicity. Paper-6837006. In vivo and in vitro data support a model in which CD28 costimulation activates AKT to phosphorylate NF90 at Ser647 and phosphorylation triggers NF90 to relocate to the cytoplasm and stabilize IL-2 mRNA. Paper-12666769. Treatment of BMCs with high-dose interleukin-2 ( IL-2) for 1 week followed by PMA plus ionomycin resulted in a lymphocyte population in which 50% and 3% of cells expressed GM-CSF and IL-3 mRNA, respectively. Paper-6234563. Retroviral gene therapy can restore immunity to infants with X-linked severe combined immunodeficiency (XSCID) caused by mutations in the IL2RG gene encoding the common gamma chain (gammac) of receptors for interleukins 2 ( IL-2), -4, -7, -9, -15, and -21. Paper-13308602. It could be shown that 1) the small amounts of IL-2 in the monocyte-T cell conditioned medium would drive DNA synthesis, but that 2) higher levels of IL-2 (20 to 100 U/ml) were needed to induce IFN-gamma, as well as the mRNA for IL-4 and the p55 IL-2R. Paper-6451063. In contrast to the results observed in T cells, IL-6 and IL-2 could enhance CD3- large granular lymphocyte (LGL) NK activity, but IL-6 either alone or in combination with IL-2 had no effect on constitutive PFP mRNA expression in resting LGL. Paper-6837006. The exocyclic derived from CDR3 (residues 82-89) of human CD4, which specifically associated with CD4 on the T cell surface to create a heteromeric CD4 complex, blocked IL-2 production and antagonized the normal function of the CD4 receptor. Paper-1474025. These results suggest that IL-2 activated human NK lysis of porcine xenografts may be inhibited by strategies which increase PAEC expression of SLA class I molecules, introduce HLA class I genes into PAEC, or use soluble HLA class I peptides. Paper-1702433. Expression of CD71, STAT3 and perforin decreased simultaneously with cytotoxicity and dose-dependently when sHLA-G1 (1.6 mug/mL-1.6 ng/mL) was added to IL-2 stimulated cultures. sHLA-G1 did not induce apoptosis and CD25 expression was not affected. Paper-12298716. A3AR and NF-kappaB levels were also analyzed in phytohemagglutinin (PHA) and lipopolysaccharide (LPS)- stimulated PBMC in the presence and absence of antibodies against interleukin 2 ( IL-2) and tumor necrosis factor-alpha ( TNF-alpha). Paper-12402344. To distinguish the affinity conversion model and the binary complex model we have carried out kinetic studies on the IL-2 binding to the high affinity IL-2-R on T lymphocytes expressing various numbers of L chains and a relatively constant number of H chains. Paper-6008573. RESULTS: Fifty-two percent of the patients mobilized with IL-2 at the maximum tolerated dose reached the target number of CD34(+) cells for transplantation with three aphereses compared to 93% of control patients who were mobilized with G-CSF alone. Paper-2174028. When PBMC were cultured up to 3 weeks with IL-2 releasing LC89 cells ( LC89/ IL-2), the number of viable CD3+ and CD56+ lymphocytes was much greater than in cultures with parental cells or with LC89 cells transduced with the other cytokine genes. Paper-828336. P-gp on lymphocytes is induced by activation with cytokines such as IL-2, IL-4 and TNF-alpha, resulting in active efflux of corticosteroids from cytoplasm of lymphocytes, which mechanisms could lead to drug-resistance and high disease activity. Paper-12297769. T lymphocytes present in thyroid infiltrates of 6 patients with Hashimoto's thyroiditis ( HT) and of 4 patients with Graves' disease (GD) were analyzed at clonal level and their profiles of mitogen- induced lymphokine secretion were characterized. Paper-6175424. Our results indicate that sequential assessment of lymphokine- activated killer activity may be a predictor of hepatocellular carcinoma and that the depression of immune function in cirrhotic patients is a serious risk factor for hepatocellular carcinoma emergence. Paper-7551579. In contrast, IFN-gamma, IL-2 and TNF-alpha inhibited the ability of thyroid lymphocytes from patients with Graves' disease and Hashimoto's thyroiditis to synthesize autoantibodies to thyroid peroxidase ( TPO) and thyroglobulin ( Tg). Paper-6536916. Finally, we show that exogenous IL-2 also has a stimulatory effect on the NK-like or lymphokine-activated killer activity, which is always concomitantly induced in virus-specific CTL generation cultures, but has no influence on the levels of IFN produced in such cultures. Paper-5432594. Finally, we demonstrate that the IL-2 toxin- mediated inhibition of protein synthesis in both human and murine T cells that bear the high affinity IL-2-R is due to the classic diphtheria toxin fragment A- catalyzed ADP ribosylation of elongation factor 2. Paper-6101311. Together, these results show that ALX exerts its effect on IL-2 up-regulation in the cytoplasm and suggest an intricate relationship between the nuclear localization/export, phosphorylation, and activity of ALX in response to TCR and CD28 signaling. Paper-11474498. As a functional consequence of this PLD2-dependent MAPK activation, interleukin-2 production evoked by PMA/ ionomycin stimulation or CD3/CD28 engagement was enhanced in the two T-cell lines overexpressing PLD2. Paper-14321459. The results shown here demonstrate that in addition to the mature 25 kDa form of TGF-beta 2, glioblastoma cells release a biologically active high molecular weight form of TGF-beta 2 which suppresses the interleukin-2-dependent growth of a T helper cell line. Paper-6907574. Among the clinical effects of IL-2, we previously reported thrombocytopenia and IL-2- induced in vitro inhibition of platelet aggregation accompanied by rapid secretion of alpha-granule components such as platelet factor 4 ( PF4) and beta-thromboglobulin. Paper-415916. The present studies examined the relationship between the CD4 cell count and three functional assays: T cell colony formation in semisolid media, the capacity of PHA- stimulated cells to express IL-2 receptors, and their ability to synthesize and secrete IL-2. Paper-6141895. Furthermore, the addition of exogenous IL 2 to standards and experimental samples was necessary to ensure that the concentration of IL 2 was similar in all samples, since IL 2 directly stimulated the proliferation of 32Dcl cells and increased their responsiveness to G-CSF. Paper-5802962. The data provide a novel insight into the mechanisms of CD4 mAbs immunosuppresssion that associates a decrease of IL-2 expression with an IL-2 resistant blockade of the progression of activated CD4+ T cells from the G1 to the S phases of the cell cycle. Paper-732895. In cytotoxicity assays, ISG15 was a potent inducer of cytolytic activity directed against both K562 (100 lytic units per 10(6) cells) and Daudi (80 lytic units per 10(6) cells) tumor cell targets, indicating that ISG15 enhanced lymphokine-activated killer-like activity. Paper-467897. Analysis of the accumulation of mRNA-encoding members of the AP-1 transcription factor family demonstrated that c-fos and junB are also expressed upon stimulation of NK and T cells with IL-2, but not IL-12, whereas expression of c-jun and junD is not modified by either cytokine. Paper-763627. Vav1 and PKCtheta also cooperated to induce transcription of reporter genes controlled either by AP-1 binding sites or the CD28RE/AP composite element contained in the IL-2 promoter by stimulating the binding of transcription factors to these two elements. Paper-8975873. Our results suggest that the TH functions assessed by IL-4 production replace the normally dominant TH function of antigen- stimulated IL-2 production in the progression toward AIDS, and raise the possibility of cytokine cross-regulation in AIDS therapy. Paper-7681570. In addition to inhibiting CD3/ CD28- induced IL-2 mRNA expression, DN-MEKK-1 abrogated the transcriptional activation of the IL-2 promoter and the distal nuclear factor of activated T cells (NFAT)-activating protein 1 (AP-1) response element in that promoter. Paper-777246. Lymphokine activated killer cells from umbilical cord blood show higher antitumor effect against anaplastic astrocytoma cell line ( U87) and medulloblastoma cell line (TE671) than lymphokine activated killer cells from peripheral blood. Paper-10281117. CONCLUSION: Our results demonstrated that IL-2 selectively enhanced production of IL-10 in HOZOT primarily through activation of STAT5, which synergistically acts with NF-kappaB/NFAT activation, implying a novel regulatory mechanism of IL-10 production in Treg cells. Paper-12698485. These results strongly show that CD27/ CD70 interaction directly enhances NK activity in the presence of IL-2 or IL-12 by increasing the effector and target conjugate formation, indicating that CD27/ CD70 interaction plays an important role in the cytotoxic function of NK cells. Paper-602739. In the added presence of the lipid-protein complex ( LPC) derived from burned skin, PHA and ConA produced much less bioavailable IL2, the combination with PHA being more inhibitory of its production than that with ConA at concentrations of 1 microgram and 5 micrograms lectin/ml. Paper-7125110. It is possible to induce apoptosis of the allo-antigen specific T cells of grafts activated by allo-antigen by exogenous Fas ligand expressed on recipient cells and this might provide a new approach for preventing GVHD and IL-2 may be more suitable for clinical application. Paper-10662255. While tetanus toxoid antigen alone induced a typical Th1-like cytokine pattern with high levels of IL2 and IFN gamma, equivalent or antibody-excess immune complexes induced a marked secretion of IL6 and IL10 while failing to induce IL2 and IFN gamma secretion. Paper-922809. Thus, the inclusion of IL-2 or TGF-beta in MLC performed with purified responder T cells resulted in outgrowth of cells secreting IL-2 and IFN-gamma, whereas addition of IL-4, IL-10, or anti-TGF-beta encouraged outgrowth of cells secreting IL-4 and IL-10. Paper-732893. Crosslinking of Ti molecules by either the appropriate nominal antigen/ MHC specificity or anti-clonotypic monoclonal antibody results in clonal expansion of such cells via induction of IL-2 receptor expression, endogenous IL-2 release and IL-2- IL-2 receptor interaction. Paper-4764233. Whereas mAb antiTac and H-31 with reactivity to the IL-2R alpha-chain ( p55) compete only partially for the IL-2-induced proliferation of these cells, mAb TU27, specific to the IL-2R beta-subunit ( p75), inhibits such growth completely even at high concentrations of IL-2. Paper-6680792. We studied the feasibility, safety, and immunologic efficacy of an IL-2- and CD40L- expressing recipient-derived tumor vaccine consisting of leukemic blasts admixed with skin fibroblasts transduced with adenoviral vectors encoding human IL-2 ( hIL-2) and hCD40L. Paper-10821483. Thus, IL-18 enhances IFN-gamma production through an IL-12-dependent pathway and exhibits synergism when combined with IL-2 in terms of enhanced IL-13 and IFN-gamma production, suggesting the involvement of IL-18/IL-12/ IL-2 pathway in modulating Th1/Th2 cytokine response. Paper-10232976. RFVP/ IL-1ra appeared beneficial in the model of ulcerative colitis represented by IL-2-/- mice (knock-out for the interleukin-2 gene), as shown by the body weight increase of IL-2-/- mice locally treated with S. gordonii producing RFVP/ IL-1ra. Paper-10150988. RESULTS: In vitro IL-2 treatment produced a rapid and dose-dependent increase in P-STAT5 within normal PBMC that correlated with the induction of transcript for the IL-2-responsive genes CIS, Pim-1, and SOCS1 (correlation coefficients 0.8628, 0.6667, and 0.7828, respectively). Paper-12256233. Analysis of VH3 genes from cultured cells by reverse transcription-polymerase chain reaction (RT-PCR)-based single-strand conformation polymorphism indicated that the combination IL-10 + IL-1beta + IL-2 promoted active V gene mutation whereas IL-10 + IL-7 + IL-4 was ineffective. Paper-8536248. However, cells activated in the presence of TGF-beta 1 proliferated vigorously in secondary cultures and produced highly elevated amounts of IL-2 (12 +/- 3-fold enhancement of IL-2 production in response to CD2 plus CD28 stimulation compared with control cells, mean +/- SEM; n = 10). Paper-138255. Subsequent progression into the S phase is mediated via both IL-2-dependent and IL-2-independent mechanisms and, although in the absence of IL-2 the majority of T cells are arrested at the G1/S transition, a significant fraction of them progresses into the S phase. Paper-2061557. These observations suggest that SHP-1 normally functions to antagonize the IL-2 signal transduction pathway and that HTLV-I infection and oncogenic transformation can lead to loss of SHP-1 expression resulting in constitutive activation of IL-2 regulated T cell responses. Paper-1390462. These results show for the first time that in fresh human monocytes, IL-8 expression is differentially regulated by IL-2 and IFN-gamma and suggest that the interactions among IL-2, IL-8, and IFN-gamma may be important for the development and control of the inflammatory response. Paper-7656822. The IFN-alpha induced inhibition of IL-2 induced proliferation in activated T-lymphocytes, was associated with a suppressed Jak3 protein expression as well as an inhibited prolonged Stat5 DNA binding, and a partially reduced expression of the Stat5 inducible gene IL-2R alpha. Paper-9353604. These findings indicate that when normal human T cells are stimulated in vitro in a manner that approximates a physiologic interaction with Ag in vivo, rIL-4 provides a potent inhibitory signal to IL-2 responsive cells that is likely mediated by IL-4-induced inhibition of IL-2R expression. Paper-6501718. These observations suggest that p70/75 IL-2 binding molecules are induced in human B-cells in the presence or absence of Tac antigen by SAC stimulation and these determinants play an important function in the transduction of IL-2 associated signal for B cell differentiation. Paper-5791713. Furthermore, the generation of double transfectants simultaneously expressing scFv-CD28 and scFv-CD3 zeta chimeras demonstrates that antigen-specific co-stimulatory signals can also synergize with signals mediated through chimeric CD3 zeta chains to secrete maximal levels of interleukin-2. Paper-749784. IL-12 augmentation of proliferation and cytotoxicity of CD8+ T cells was not inhibited by a mAb to the p55 subunit of the IL-2 receptor (alpha-Tac) at a concentration sufficient to block the activity of exogenously added IL-2, indicating that the activity of IL-12 did not require IL-2. Paper-7589274. Thus, the increased expression of the IL-2Rbeta is critical for the synergistic activation of gammadelta T cells by IL-12 plus IL-2; it is also probable that at least the low-affinity IL-12R contributes to the activation of gammadelta T cells mediated by either IL-12 alone or IL-12 plus IL-2. Paper-1721809. Functional studies performed with alloreactive natural and lymphokine activated killer cells as well as antigen-specific CD8+ T cell populations demonstrated that HLA-G expression inhibits lysis of RCC cells by these different immune effector cells, whereas HLA-G- normal kidney cells were recognized. Paper-10204226. When rhIL-1 was administered within 24 h after SEB inoculation, the cytokine interfered with tolerance induction; V beta 8+CD4 T cells from mice that had been treated with both SEB and IL-1 proliferated in response to SEB and produced IL-2, IL-4, and IFN-gamma upon TCR/ CD28 cross-linking. Paper-407684. The repressive effect of Nur77 on IL-2 promoter activation is mediated through inhibition of the transcription factor complex nuclear factor-kappaB ( NF-kappaB), since blocking or alteration of the IL-2 NF-kappaB binding sites resulted in abrogation of the repressive effect of Nur77. Paper-10659971. It is concluded that: 1) both T cells lacking and T cells having receptors for IL 2 produce IL 2, but only IL 2 receptor-negative T cells appear to secrete IL 3; and 2) virtually all of the T cells that produce IFN-gamma after PHA stimulation express receptors for IL 2. Paper-4638304. Recently, interleukin 2 ( IL-2) has been shown to induce increased activity of the p56lck protein-tyrosine kinase ( PTK) in T-cell and natural killer cell lines, and evidence for a direct interaction between the p75 subunit of the IL-2 receptor (IL-2R) and this src-family kinase has been reported. Paper-7334362. The production of interleukin 1 (IL-1) and interleukin 2 ( IL-2) by peripheral blood mononuclear cells (PBMC) stimulated with human myelin basic protein ( MBP) was assessed in vitro in multiple sclerosis ( MS) patients in relapse, patients with other neurological diseases (OND) and healthy subjects. Paper-6114254. Our current findings indicate that SR asthma is associated with a dysregulation of the expression of the genes encoding for Th2/Th1 cytokines in airway cells and is compatible with the concept that a combination of IL-2 and IL-4 induce glucocorticoid ( GR) binding affinity and T cell responsiveness to glucocorticoids. Paper-146263. Comparison of IL-4-driven versus IL-2-driven T-cell responses demonstrated that IL-2 was able to upregulate mRNA for IL-4 receptors and interferon-gamma, while IL-4 had minimal effects on upregulating mRNA for either the p55 or the p75 IL-2 receptor subunits or interferon-gamma. Paper-7706461. Low doses of PT induced ADP-ribosylation of G proteins but this treatment did not affect significantly PHA- induced [Ca2+]i increase and IL-2- induced DNA synthesis suggesting that the substrates of the ADP-ribosyltransferase activity of PT are not involved in the signalling pathways leading to DNA replication. Paper-39763. Patients' peripheral blood leukocytes (PBL) were tested before, during, and after therapy with rCD4-IgG for T helper ( TH) cell function assessed by antigen- and mitogen- stimulated proliferation and interleukin-2 production in response to influenza A virus, allogeneic PBL (alloantigens), and phytohemagglutinin. Paper-7668890. Productive engagement of T cells by antigen-presenting cells (APCs) results in recruitment of PKC theta to the T cell-APC contact area--the immunological synapse--where it interacts with several signaling molecules to induce activation signals essential for productive T cell activation and IL-2 production. Paper-9195420. Interferon-gamma ( IFN-gamma), interleukin 2 ( IL-2) and granulocyte/macrophage colony- stimulating factor ( GM-CSF) were detected in the culture supernatant after 72 hours incubation with trichophytin in the peripheral blood mononuclear cells (PBMC) obtained from a patient who had a dermatophyte infection. Paper-7550327. The combination of IL-4 and low dose IL-2 still significantly improved the total MN cell recovery but did not modify the distribution of T and NK lymphocytes; IL-4 inhibited low dose IL-2- induced NK and LAK cell activity, and increased the BL-esterase activity induced by high or low dose IL-2. Paper-6829684. OBJECTIVE: Interferon-gamma ( IFN-gamma) and interleukin-4 ( IL-4) production of ovalbumin- stimulated and interleukin-2 (IL-2)-stimulated peripheral blood mononuclear cells from egg-sensitive patients was investigated and compared with that of stimulated peripheral blood mononuclear cells from nonatopic healthy children. Paper-615503. Numbers of IL-2 secreting cells were higher in MS patients compared to patients with AM + TH after stimulation with myelin proteolipid protein ( PLP), myelin associated glycoprotein ( MAG) and myelin oligodendrocyte glycoprotein ( MOG), but not after stimulation with myelin basic protein ( MBP). Paper-7759304. A simple model system based on the effect of FK 506 on isolated rat pancreatic islets was utilised to study the relationship between inhibition of insulin biosynthesis, inhibition of interleukin 2 ( IL-2) activation and FK binding protein ( FKBP-12) binding of FK 506 and a number of FK 506 analogues. Paper-509967. The enhancement of ADCC activity was blocked by the addition of an antibody against hrIL-6 but not by an antibody to the IL-2 receptor (capable of blocking the induction of lymphokine- activated killer cell cytotoxicity by IL-2), suggesting that hrIL-6 augmentation of ADCC activity may not be mediated through IL-2. Paper-6923725. T cell clones derived from cerebrospinal fluid (CSF) of patients with multiple sclerosis ( MS) were analysed for their capacity to produce interleukin 2 ( IL-2), interleukin 4 ( IL-4), interferon-gamma ( IFN-gamma) and tumor necrosis factor-alpha ( TNF-alpha). Paper-7407924. The results showed that the combined transcriptional regulatory sequences of E(AFP)-P(ALB) could control the targeted expression of cytokine genes in AFP-positive human HCC cells, and the expression level of the IL-2/IFNalpha2b fused gene was positively correlated to the level of AFP expression in the infected cells. Paper-1792134. This interaction with T-cell-specific transcription factors indicates an important immunomodulatory role for PPARgamma in T lymphocytes and could suggest a previously unrecognized clinical potential for PPARgamma ligands as immunotherapeutic drugs to treat T-cell- mediated diseases by targeting IL-2 gene expression. Paper-2133901. Additionally, upon overexpression, the ALX NES mutant was found to be impaired in inhibiting TCR/ CD28- induced transcriptional up-regulation of the RE/AP composite element from the IL-2 promoter, whereas a truncated form of ALX that is a potent inhibitor of RE/AP activation was found to reside entirely in the cytoplasm. Paper-11474498. Human CD4(+) T cells were thus recovered from the HIV-DC-immunized hu-PBL-SCID mice and were re-stimulated in vitro by co-culture for 2 days with autologous adherent PBMC as antigen presenting cells, APC previously pulsed with inactivated HIV in IL-2-containing medium to expand HIV-1-reactive CD4(+) T cells. Paper-11515902. Thus, by pharmacologic, genetic, and biochemical criteria in vitro and in vivo, our results suggest that IL-15 and IL-2 oppositely regulate CX3CR1 gene expression by differentially recruiting NFAT1 and NFAT2 to a kappaB-like NFAT site within the CX3CR1 promoter. Paper-10630708. However, proliferation of TH2 cells is enhanced by IL-2 pretreatment, while the TH1 clones or CTL clones through the T cell receptor (TCR) profoundly inhibits IL-2-induced proliferation of those cells, whereas such stimulation either has very little effect or augments the proliferation of IL-4-producing clones. Paper-11964814. We have found that IL-2 induces association of SHP-1 with the IL-2 receptor complex, and that once SHP-1 is recruited to the activated receptor it is able to decrease tyrosine phosphorylation of IL-2Rbeta and the associated tyrosine kinases Jak1 and Jak3. Paper-1390462. Gamma interferon produced by activating T cells in allo- or auto-MLR can reproduce T cell-mediated regulation of EBV-induced B cell proliferation, and the failure of RA auto-MLR to generate that lymphokine parallels the defective T cell regulation of EBV- induced B cell proliferation characteristic of RA lymphoid cells. Paper-4408636. In addition, the activation of large granular lymphocytes to lymphokine- activated killer cells mediated by IL-T-containing conditioned medium was not blocked by antibodies directed toward IL-2 or IL-2 alpha but was inhibited by an antibody to IL-2R beta, suggesting the requirement of this receptor subunit for IL-T action. Paper-121599. The addition of 20 U/ml of recombinant interleukin-2 at the initiation of suppressor coculture bioassays completely neutralizes the suppressive effect of suppressor T cells exerted on CD8-positive responder T cells, but does not restore expression of transferrin and interleukin-2 receptors on CD4-positive T cells. Paper-6386770. Using a cDNA-polymerase chain reaction ( PCR) with specific primer sets for the various CSF, we showed that IL-2 treatment induced the expression of mRNA for M-CSF, GM-CSF, IL-3, and IL-5, but not for granulocyte CSF (G- CSF) in peripheral blood mononuclear cells, suggesting differential expression of CSF in vivo in response to IL-2. Paper-6913638. Cells cultured in the presence of IL-2 or IL-15 secreted comparable amounts of interferon-gamma and IL-2 in response to melanoma cells in vitro and were phenotypically similar in terms of costimulatory molecules ( CD27 and CD28), cytokine receptors ( CD25, CD122, and CD127), and a lymphoid homing molecule ( CD62L). Paper-12004967. These studies have established that activation caused a rapid increase in the formation of GTP-bound Ras, which stimulates the mitogen-activated protein kinase pathway involving the extracellular- regulated kinase-2 ( ERK-2) and activates the nuclear factor of activated T cells (NF-AT) that regulates interleukin-2 ( IL-2) gene transcription. Paper-1999500. While the inhibitory activity of IL-1-induced proliferation was stable, that of IL-2- and IL-3- induced proliferation was abrogated within a week at 4 degrees C. Inhibition of IL-2-dependent growth was also observed using human IL-2-dependent cells, but the growth of other factor-independent human hematopoietic cell lines was not affected at all. Paper-6213312. These synonyms are used for gene IL2 (interleukin 2): TCGF, T-cell growth factor, lymphokine, Interleukin-2, IL-2. These accession numbers are used for gene IL2: Q9C001 (UNIPROT__AC), Q7Z7M3 (UNIPROT__AC), AAK26665 (NCBI_GENBANK__AC), AAA98792 (NCBI_GENBANK__AC). IL2 is a homologue of IL2 (interleukin 2) from Bos taurus. IL2 is a homologue of IL2 (interleukin 2) from Pan troglodytes. IL2 is a homologue of IL2 (interleukin 2) from Canis lupus familiaris. IL2 is a homologue of Il2 (interleukin 2) from Mus musculus. IL2 is a homologue of Il2 (interleukin 2) from Rattus norvegicus. Important links ! iHOP - Information Hyperlinked over Proteins . Concept & Implementation by Robert Hoffmann. |