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Phosphatidyl inositol 3-kinase ( PI3K) is activated by IL-2. Paper-1240722.
A specific inhibitor of TAK1 blocked production of IL-2. Paper-11445907.
Protein kinase B ( PKB) is activated by IL-2 via PI3K. Paper-1240722.
Lymphokine- activated killer cell activity in rheumatoid arthritis. Paper-5489221.
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.
However, IL-2- mediated Jak3/Stat activation is not dependent on Lck or Syk. Paper-8463746.
However, IL-2- induced activator protein-1 ( AP-1) is oxidation-sensitive. Paper-8612699.
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.
Herein, we demonstrate that PKB is activated by IL-2 in a PI 3-kinase-dependent fashion. Paper-1038450.
Thrombopoietin and interleukin-2 induce association of CRK with STAT5. Paper-8612674.
In addition, IL-2 and IL-12 synergize with sCD23 to induce TNF-alpha production. Paper-129932.
Interleukin-8 suppresses the toxicity and antitumor effect of interleukin-2. Paper-108566.
Even low, nonmitogenic concentrations of recombinant IL-2 stimulated IL-3 release. Paper-4857332.
Role of interleukin-18 in human natural killer cell is associated with interleukin-2. Paper-15522608.
This finding was likely due to IL-2- induced CCR5 expression on CD4+ thymocytes in FTOC. Paper-11536549.
Treatment with IL-2 with or without IFNalpha significantly suppressed serum DPP IV activity. Paper-8729036.
Anti- IL-10 antibody reversed almost completely the gp41 inhibitory effect on IL-2 production. Paper-1377045.
Dendritic cell-derived IL-2 production is regulated by IL-15 in humans and in mice. Paper-11016797.
The augmentation of IL-8 mRNA by IL-2 was associated with an increase in IL-8 secretion. Paper-7656822.
Treatment of T lymphocytes with IL-2 promotes p56lck kinase activity. Paper-7193167.
The factor did not inhibit IL 2- induced or other proliferative responses not related to IL 1. Paper-5179098.
In these experiments, anti- LFA-1 mAb markedly up-regulated the lytic ability of IL-2-cultured PBL. Paper-7301119.
Anti- beta 2m has no effect on mitogen- induced cell proliferation and IL 2 production. Paper-5133017.
It is demonstrated that anti- beta 2m antibodies inhibit the production of interleukin 2 ( IL 2). Paper-5133017.
The frequency of IL-2- secreting cells and CD4/ CD8 ratio in BALF had a weak positive correlation. Paper-8842662.
Effects of the multiple sclerosis associated -330 promoter polymorphism in IL2 allelic expression. Paper-10373286.
The levels of the growth and cytotoxic activity induced by IL-7 were similar to those induced by IL-2. Paper-989103.
Using chromatin immunoprecipitation, BACH2 was shown binding to the human IL-2 proximal promoter. Paper-13510945.
Likewise, priming for IFN-gamma production could be blocked by CTLA4-Ig and reversed by IL-2. Paper-108292.
Carboxy-terminal truncated STAT5 is induced by interleukin-2 and GM-CSF in human neutrophils. Paper-9236908.
However, a greater dose of IL-15 is needed to reach the same level of proliferation stimulated by IL-2. Paper-1473851.
The presence of IL-2- induced GM-CSF and M-CSF was also demonstrated by specific radioimmunoassays. Paper-6913638.
Mechanism of HDAC inhibitor FR235222- mediated IL-2 transcriptional repression in Jurkat cells. Paper-13413887.
IL-8 also stimulated IL-2 production (by up to 42%) and CD69 expression, although weakly (+27%). Paper-2206280.
Our results indicate that DC-produced IL-2 is tightly coregulated with the expression of IL-15. Paper-11016797.
In addition, murine as well as both human IL 1 proteins stimulate IL 2 production by EL-4 cells. Paper-5147250.
Protein phosphatase 2A regulates interleukin-2 receptor complex formation and JAK3/ STAT5 activation. Paper-14228943.
CONCLUSIONS: SLC and IL-2 were produced by autocrine in DCs transfected with SLC and IL-2 genes. Paper-14051959.
Interleukin 2 regulates the activity of the lyn protein-tyrosine kinase in a B-cell line. Paper-7334362.
The production of both IL-1 and IL-2 was stimulated by a nanomolar concentration of CRF by itself. Paper-6768881.
IL-2 up-regulates but IFN-gamma suppresses IL-8 expression in human monocytes. Paper-7656822.
Interleukin 2-dependent release of interleukin 3 activity by T4+ human T-cell clones. Paper-4857332.
Unlike CIS, SOCS-3 was rapidly tyrosine phosphorylated in response to IL-2. Paper-1908920.
Protection of cultured human monocytes from lymphokine- activated killer- mediated lysis by IFN-gamma. Paper-5957640.
IL-2- induced IL-9 production by allergen-specific human helper T-cell clones. Paper-13372646.
SOCS2 can enhance interleukin-2 ( IL-2) and IL-3 signaling by accelerating SOCS3 degradation. Paper-10979446.
These results shown that PSK and IL-2 produce different variations in PKC isoenzymes and MAPK in NKL cells. Paper-9661279.
Five U/ml of IFN-gamma induced IL-2R alpha mRNA and 2.2 nM of IL-2 induced IL-2R beta mRNA, both within 3 h. Paper-73221.
IL-1 inhibits while IL-2 stimulates the growth of the androgen-sensitive LNCaP cell line. Paper-1665732.
However, no evidence could be found that FOXP3+ cells actively suppress IL2 expression by FOXP3- cells. Paper-14291659.
Down-modulation of IL-2- triggered JAK3- STAT5 signaling following CD4-ligand binding. Paper-1790854.
These data show P-gp mediated transmembrane flux of IL-2 in T lymphocytes and HCT-8 cells. Paper-661406.
Shock waves increase T-cell proliferation or IL-2 expression by activating p38 MAP kinase. Paper-10932538.
IL-5 production was observed in MNCs from lung cancer patients stimulated with IL-2, but not with IL-15. Paper-1555954.
The IL-7 stimulatory effect appears to be mediated via both an IL-2 pathway and an IL-7-independent pathway. Paper-7415758.
In vivo therapy of hepatocellular carcinoma with a tumor-specific adenoviral vector expressing interleukin-2. Paper-1315482.
Finally, proliferation induced by both IL-2- and IL-3 was significantly inhibited in the presence of SOCS-3. Paper-1908920.
We then showed that AMPK inhibition reduced PMA/Io- induced IL-2 mRNA expression and IL-2 promoter activation. Paper-14714266.
Human activated CD4(+) T lymphocytes increase IL-2 expression by downregulating microRNA-181c. Paper-15600684.
Moreover, IL-10 effects on the early G1 proteins p27(Kip1) and cyclin D2 were similarly reversed by exogenous IL-2. Paper-1705894.
Associated with the inhibition of the cell cycle, IL-10 suppressed SEB induction of interleukin-2 ( IL-2). Paper-1705894.
We found that NFATc2 and cJun are exclusive in their ability to synergistically activate human IL-2 transcription. Paper-15351482.
Phosphorylation at Ser647 of NF90 up-regulated IL-2 production in response to CD28 costimulation. Paper-12666769.
Schnurri-3 (KRC) interacts with c-Jun to regulate the IL-2 gene in T cells. Paper-10357587.
Lymphokine- activated killer cells can discriminate CD34+ leukemia cells from normal hematopoietic progenitor cells. Paper-564536.
Lymphokine- activated killer activity and natural killer activity in hepatocellular carcinoma patients were assessed. Paper-6246401.
Although ILF bound constitutively to the IL-2 promoter, it was not detected as a component of the NFAT complex. Paper-952078.
Interestingly, the transfection of JAR cells with HLA-G completely eliminates the growth-inhibitory effect of IL-2. Paper-1886435.
Suppressor and cytolytic cell function in multiple sclerosis. Effects of cyclosporine A and interleukin 2. Paper-5148301.
Interleukin 2 ( IL2) alone had a restorative effect which could be considerably (10X) enhanced by IFN-alpha. Paper-6109114.
Lymphokine- activated killer activity was impaired in hepatocellular carcinoma as compared to that in normal subjects. Paper-6246401.
IL-2 mRNA expression in lymphocytes was not different between PHA control and the cultures with P-gp inhibitors. Paper-661406.
Interleukin-2 ( IL-2) rapidly activated Stat5 in fresh PBL, and Stat3 and Stat5 in preactivated PBL. Paper-209479.
X-ray crystal structure of proto-oncogene product c-Rel bound to the CD28 response element of IL-2. Paper-8958913.
CD28-responsive element/activator protein-1-binding site (RE/AP) within the IL-2 promoter was a functional target for TAK1. Paper-11445907.
By contrast concentrations of PRL five- to tenfold the physiological levels inhibited the mitogenic response to IL2 and PHA. Paper-7468652.
These results suggest that the Pgp efflux pump may be involved in the transport of IL-2 in T lymphocytes. Paper-631772.
Our data show an increased IL2 expression among GT and TT genotypes previously associated with susceptibility to MS. Paper-10373286.
We have recently reported that IL 2- activated killer (LAK) cells are capable of lysing cultured human monocytes. Paper-5957640.
Moreover, pharmacological abrogation of Lck activity did not inhibit IL-2- mediated phosphorylation of Jak3 and Stat5a. Paper-8463746.
The C-terminal region of human NFATc2 binds cJun to synergistically activate interleukin-2 transcription. Paper-15351482.
IL-10 also inhibited expression of IL-2 transcriptional regulators c-fos and c-jun, which also inhibit other cell functions. Paper-1705894.
Defective function of lymphokine- activated killer cells and natural killer cells in patients with hepatocellular carcinoma. Paper-6246401.
Moreover, expression of this C-terminal region of NFATc2 specifically repressed the synergistic activation of IL-2 transcription. Paper-15351482.
IL-1 promotes the neuroendocrine phenotype and IL-2 promotes the exocrine phenotype in prostate cancer. Paper-1665732.
These results establish a crucial PI3K/ PKB- mediated link between the IL-2 teceptor and the cell cycle machinery. Paper-1240722.
Our previous study of interleukin-2 ( IL-2) signaling found that redox factor-1 ( Ref-1) mRNA was upregulated by IL-2. Paper-8612699.
An anti- MUC1-antibody- interleukin-2 fusion protein that activates resting NK cells to lysis of MUC1-positive tumour cells. Paper-10034723.
Reduction of serum CRP or IL-6 levels with thalidomide may enhance the responsiveness of renal cell carcinoma to IL-2. Paper-10239539.
These data suggest that IL-2 must stimulate both Erk2 activity and a further pathway(s) to trigger cell proliferation. Paper-99834.
IL-2 and IL-15 each mediate de novo induction of FOXP3 expression in human tumor antigen-specific CD8 T cells. Paper-13168827.
CD4+ CD45RA+ T cells modulate allergen- induced interleukin 2 responsiveness in human lymphocytes. Paper-7264623.
Recombinant interleukin 3 induces interleukin 2 receptor expression on early myeloid cells in normal human bone marrow. Paper-7210334.
AIDS-related Burkitt's-type lymphomas are a target for lymphokine- activated killers induced by interleukin-2 and prolactin. Paper-771451.
This suggested that Epo binding caused the activation of an IL-2 signal pathway mediated by the chimeric receptors. Paper-345059.
The augmented migratory capacity of IL-2- activated versus resting NK cells was associated with increased CCR2 transcript levels. Paper-1089285.
Suppression of human monocyte function against Candida albicans by autologous IL-2- induced lymphokine-activated killer cells. Paper-22583.
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.
Interleukin 2-dependent and interleukin 2-independent pathways of regulation of thymocyte function by interleukin 6. Paper-6008740.
Furthermore, the cells in the MS lesion expressed the interleukin 2 ( IL 2) receptor, as identified by the anti-TAC monoclonal antibody. Paper-5394810.
Recombinant human erythropoietin stimulates production of interleukin 2 by whole blood cell cultures of hemodialysis patients. Paper-10568163.
GAPDH mRNA is induced two- to fivefold over resting levels upon IL2 stimulation, due in part to an increased rate of transcription. Paper-6532053.
Furthermore, highly purified CD8- T cells can be activated by IL-6 in the presence of Con A to secrete IL-2. Paper-5492416.
Our data demonstrate that the p75 chain is expressed on human monocytes and is involved in the activation of monocytes by IL-2. Paper-6538524.
To test this hypothesis, we investigated whether IL-2 gene polymorphisms and its serum levels are associated with NPC in a Chinese population. Paper-15216863.
PHA induces IL-2 receptors on B-CLL cells and is a potential biological response modifier for the LIL-2-diphtheria toxin, DAB486IL-2. Paper-112302.
Induction of this IL-2 promoter binding factor occurred concomitantly with the induction of NF-90 and translocation of NF-90 to the nucleus. Paper-10134262.
Preferential re-uptake of externally derived PRL by IL-2- stimulated NK cells was also indicated by up-modulation of the PRL receptor. Paper-866285.
We also observed that interleukin-2 ( IL2) production induced via CD28 triggering was sensitive to a selective protein kinase C inhibitor. Paper-7892871.
Systemic lupus erythematosus serum IgG increases CREM binding to the IL-2 promoter and suppresses IL-2 production through CaMKIV. Paper-10776182.
In contrast, no IL-2 activity could be detected in supernatants of CMV-stimulated MNC cultures, whereas PHA induced normal IL-2 production. Paper-5926903.
We report here that p38 is specifically activated by signals that lead to interleukin-2 ( IL-2) production in T lymphocytes. Paper-1439812.
Costimulation of CD28 in T cells up-regulates IL-2 mRNA levels via transcription activation and mRNA stabilization. Paper-12666769.
NF45 ( ILF2) and NF90 ( ILF3) regulate the IL-2 gene transcription via interaction with the antigen receptor response element. Paper-12140624.
Tumor necrosis factor, interferon-gamma and interleukin-2 ( IL-2) had no effect on IL-6 synthesis in monocytes or macrophages. Paper-6025522.
High-affinity IL-2-R binding results from an exceptional type of cooperative interaction between two IL-2-binding proteins termed alpha and beta. Paper-5787536.
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.
These results suggest that AMPK mediates IL-2 production by regulating NF-AT and AP-1activation during T cell stimulation. Paper-14714266.
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.
Here, using an inducible system, we demonstrate that Nef increases IL-2 secretion from T cells stimulated via CD3 or CD28. Paper-2086704.
Decreased 4-1BB expression on HIV-specific CD4+ T cells is associated with sustained viral replication and reduced IL-2 production. Paper-13885630.
IL-2 therapy affected serum tumor necrosis factor ( TNF), interferon gamma ( IFN gamma) and soluble IL-2 receptor (sIL-2r) levels. Paper-6908437.
Transient CD86 expression on hepatitis C virus-specific CD8+ T cells in acute infection is linked to sufficient IL-2 signaling. Paper-14253239.
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.
Interleukin enhancer binding factor ( ILF) binds to the interleukin-2 ( IL-2) promoter and regulates IL-2 gene expression. Paper-9262004.
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.
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.
Enhancement of interleukin-2- induced lymphokine- activated killer activity by interleukin 7 against autologous human renal cell carcinoma. Paper-1644608.
Overexpression of either antisense CREM or CREB plasmid rescued morphine- induced inhibition of IL-2 promoter activity and protein production. Paper-13136650.
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.
T-cell proliferation and transcriptional activation of the IRF-1 gene is also induced by the cytokine interleukin 2 ( IL-2). Paper-127002.
Interestingly, the production of IL-2 by myeloid DCs is induced by T-cell- mediated stimuli and depends on the presence of IL-15. Paper-11016797.
IL-7-driven TIL growth was consistently blocked by anti- IL-2, anti-IL-2R and anti- IL-7 antibodies (37.2%, 41.6% and 82.2% suppression, respectively). Paper-7415758.
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.
Reciprocal granzyme/ perforin- mediated death of human regulatory and responder T cells is regulated by interleukin-2 ( IL-2). Paper-15105151.
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.
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.
In contrast, IFN-alpha did not enhance the effect of an IL2-free T cell-derived supernatant able to support the B cell differentiation. Paper-6109114.
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.
This inhibitor did not affect IL 2- promoted proliferation of mouse thymocytes or CT-6 cells or IL 1-promoted proliferation of human dermal fibroblasts. Paper-4772247.
We demonstrated by immunohistochemistry that BECs express MCP-1 after injury and that receptor expression can be regulated by exposure to IL-2 and LPS. Paper-9596546.
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.
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.
Janus kinase 3 regulates interleukin 2- induced mucosal wound repair through tyrosine phosphorylation of villin. Paper-12523112.
SOCS-3 is tyrosine phosphorylated in response to interleukin-2 and suppresses STAT5 phosphorylation and lymphocyte proliferation. Paper-1908920.
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.
IL-2 up-regulated TLR4 surface expression on human peripheral blood monocytes, but did not change expression on human peripheral B cells. Paper-9193739.
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.
IL-2- induced growth of CD8+ T cell prolymphocytic leukemia cells mediated by NF-kappaB induction and IL-2 receptor alpha expression. Paper-1449207.
Mutagenesis of each of the two sequence elements required for ILF binding decreased IL-2 promoter activity when assayed in transfection assays. Paper-952078.
In this transformant, we revealed that IL-2 induced erythroid differentiation and the same pattern of tyrosine phosphorylation as Epo. Paper-7326993.
Depletion of natural killer cells before culture did not inhibit low-dose IL-2- induced LAK generation or the ability of GM-CSF to augment LAK generation. Paper-7775509.
Non-cytotoxic CD4 tumour-infiltrating lymphocytes induce responses in patients with metastatic renal cell carcinoma previously treated with interleukin-2. Paper-414320.
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.
IL-9 production by Th clones stimulated with immobilized anti-CD3 Ab was significantly suppressed by the addition of anti- IL-2 neutralizing Ab into the culture. Paper-13372646.
The growth of activated human T lymphocytes in response to interleukin-2 ( IL-2) is suppressed by transforming growth factor-beta ( TGF-beta). Paper-5796256.
The results showed that anti-CD3 McAb and PHA not only enhanced the proliferation of splenocytes induced by IL-2, but also produced synergism if used simultaneously. Paper-173613.
This report addresses the role of individual IL-2 binding proteins of the IL-2 receptor in the stimulation of cell proliferation by IL-2. Paper-94245.
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 investigated the roles of B-Raf in TCR- mediated IL-2 production coupled with ERK activation in the Jurkat human T cell line. Paper-10637232.
Molecular mechanisms of regulatory T cell function: foxp3 binds to the endogenous IL-2 locus and promotes histone deacetylation in an activation-dependent manner. Paper-12227471.
In addition, IL-6 synergistically enhanced the stimulation of thymocyte proliferation by recombinant human interleukin 1 (IL-1) or interleukin 2 ( IL-2). Paper-6008740.
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.
Jak3-regulated genes: DNA array analysis of concanavalin a- interleukin-2- activated chicken T cells treated with a specific jak3 inhibitor. Paper-9634787.
Immunologically, numbers of natural killer cells were increased and natural killer and lymphokine- activated killer cell activities were augmented after IL-2 treatment. Paper-6510968.
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.
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.
High-affinity IL-2-R correspond to a membrane receptor complex composed of two different IL-2-binding proteins, the Tac antigen (alpha chain) and a 70-75 kD beta chain. Paper-5482831.
Nuclear export of NF90 to stabilize IL-2 mRNA is mediated by AKT-dependent phosphorylation at Ser647 in response to CD28 costimulation. Paper-12666769.
However, the maximum increase of lymphokine- activated killer activity in hepatocellular carcinoma was not as high as that of normal subjects or liver cirrhosis patients. Paper-6246401.
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.
When T cells were stimulated under weak stimulation conditions, pharmaceutical and molecular p38 inhibitors induced a dramatic increase of IL-2 production. Paper-11824683.
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.
Genistein, a protein tyrosine kinase inhibitor, prevents the dissociation of enzymatically active Raf-1 from the ligand- stimulated IL-2 receptor complex. Paper-66073.
TAK1- mediated transcriptional activation of CD28-responsive element and AP-1- binding site within the IL-2 promoter in Jurkat T cells. Paper-11445907.
Potential role of phospholipase D2 in increasing interleukin-2 production by T-lymphocytes through activation of mitogen- activated protein kinases ERK1/ ERK2. Paper-14321459.
Interferon-alpha and interleukin 2 synergistically enhance basic fibroblast growth factor synthesis and induce release, promoting endothelial cell growth. Paper-7880934.
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.
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.
T cells anergized by n-butyrate demonstrated reduced interleukin-2 ( IL-2) secretion and decreased activating protein 1 ( AP-1) activity upon restimulation. Paper-15062842.
Lowered serum dipeptidyl peptidase IV activity is associated with depressive symptoms and cytokine production in cancer patients receiving interleukin-2-based immunotherapy. Paper-8729036.
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 particular, we could show that DCs from IL-15-deficient mice were strongly impaired in the ability to produce IL-2 after interactions with different microbial stimuli. Paper-11016797.
The IL-2 receptor beta subunit is absolutely required for mediating the IL-2-induced activation of NK activity and proliferative activity of human large granular lymphocytes. Paper-6685479.
Nuclear factor of kappaB ( NF-kappaB) is a major transcription factor regulating the expression of interleukin-2 ( IL-2) and interleukin-2 receptor-alpha (IL-2Ralpha) in Th(1) cells. Paper-13431044.
These results reveal that the effects of IL-18 on human NK cell are associated with IL-2 concentration and suggest the importance of IL-2 level in cytokine immunotherapy. Paper-15522608.
Likewise, spontaneous lymphocyte cytotoxicity was not detectable in the leukapheresis product; lymphokine- activated killer cell activity was inducible in vitro with IL-2. Paper-876644.
The doses of TGF beta 2 that inhibit cytotoxicity of IL-2 stimulated cells by 60%-70% were much less effective when the same cells were stimulated with anti-CD3/anti-CD28/ IL-2. Paper-7639712.
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.
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.
CD28 and T cell antigen receptor signal transduction coordinately regulate interleukin 2 gene expression in response to superantigen stimulation. Paper-55961.
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.
Human immunodeficiency virus-1 envelope glycoproteins and anti-CD4 antibodies inhibit interleukin-2- induced Jak/STAT signalling in human CD4 T lymphocytes. Paper-9876970.
RESULTS: The proliferation of peripheral blood monocytes (PBMC) was inhibited by bFGF 5 micrograms.L-1. bFGF did not affect the stimulation of LAK cells induced by IL-2. Paper-2024136.
The relevant role of the IL2RA gene on MS susceptibility adds support to its common effect on autoimmune risk and the suggestive association of IL2/IL21 warrants further investigation. Paper-15167305.
Previously, we showed that low-dose interleukin-2 ( IL-2) and 13-cis-retinoic acid ( RA) improved the tumor- associated immunodeficiency and decreased VEGF in patients with AOC. Paper-14226221.
Defective lymphokine- activated killer activity was detected more than 6 mo before detection of a space occupying lesion in the liver or elevation of alpha-fetoprotein level above 400 ng/ml. Paper-7551579.
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.
Antibody to IL-2 partially inhibited both PRL- and IL-2- induced proliferation whereas antibody to PRL significantly decreased PRL but not IL-2-induced proliferation. Paper-321671.
B-Raf contributes to sustained extracellular signal-regulated kinase activation associated with interleukin-2 production stimulated through the T cell receptor. Paper-10637232.
Human recombinant IL-2 augments immunoglobulin and induces rheumatoid factor production by rheumatoid arthritis lymphocytes engrafted into severe combined immunodeficient mice. Paper-167306.
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.
Moreover, genotypes carrying the IL-2 -330 G variant allele were associated with decreased serum IL-2 levels compared with the homozygous wild-type genotype in patients with NPC. Paper-15216863.
IL-4 inhibits IL-2- induced tumoricidal activity and secretory functions of human monocytes. Modulation of IL-2 binding and IL-2 receptor beta gamma chain expression. Paper-314060.
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.
The findings suggest that when SOCS-3 is rapidly induced by IL-2 in T cells, it acts to inhibit IL-2 responses in a classical negative feedback loop. Paper-1908920.
CONCLUSION: Enhanced IL-2 production in stimulated T cells expressing HIV-Nef is associated with increased activation of PI3K-dependent signalling pathways. Paper-8748732.
NR2F6 potently antagonized the ability of T helper 0 (Th0) and Th17 CD4(+) T cells to induce expression of key cytokine genes such as interleukin-2 ( IL-2) and IL-17. Paper-12967897.
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.
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.
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.
Suppression of interleukin 2 receptor acquisition by monoclonal antibodies recognizing the 50 KD protein associated with the sheep erythrocyte receptor on human T lymphocytes. Paper-4884716.
The high affinity receptor for IL-2 is composed of at least two chains, a p55 chain that binds IL-2 with low affinity and a p75 chain that binds with intermediate affinity. Paper-7248468.
Importantly, PI 3-kinase signals are sufficient for PKB activation in IL-2-dependent T cells, and PKB is a target for PI 3-kinase signals in IL-2 activation pathways. Paper-1038450.
Finally, the augmented expression of IL-2R gamma in IL-2- and IFN gamma-treated monocytes was associated with an increased IL-2-binding activity, compared with that of unstimulated cells. Paper-120157.
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.
By gel filtration the T cell-replacing factor ( TRF) activity is present in the 30-15-kDa fraction of T cell supernatants and is associated to interleukin 2 ( IL2). Paper-5178747.
These results show that IL-2 is capable of inducing the nuclear expression of NF-kappaB in primary CD8+ T-PLL cells, and that this effect is mediated, at least in part, at a pretranslational level. Paper-1449207.
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.
Interleukin-3 ( IL-3) can promote the proliferation of certain classes of lymphocytes distinct from those that are dependent on interleukin-2 ( IL-2) for growth. Paper-4325625.
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.
These data favor a model of IL-2 receptor activation in which an IL-2- activated protein tyrosine kinase phosphorylates the IL-2 receptor and/or receptor- bound Raf-1. Paper-66073.
IL-15 displayed better target-specific accumulation and more rapid clearance from the circulation than did IL-2, and thus it can be considered to be a novel and unique therapeutic agent. Paper-8357976.
IL-2 induces the synthesis and expression of the IL-2 receptor alpha-chain ( IL-2R) on the lymphocyte as well as the release of a truncated form of IL-2R (sIL-2R). Paper-246983.
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.
These results suggest that IL-5 plays an important role in the induction of selective eosinophilia in humans and that IL-5 is produced from T cells with IL-2 stimulation. Paper-6196770.
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.
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.
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.
These results suggest that important regulatory sequences in the IL-2 promoter are bound by ILF and that this binding may be involved in the control of IL-2 gene expression. Paper-952078.
One-hour infusion of IL-2 induced a very rapid secretion of TNF-alpha, IL-6 and IFN-gamma with considerably higher peak levels than during IL-2 continuous intravenous infusion. Paper-7447351.
The addition of picogram quantities of exogenous TGF-beta to cell cultures of indolent Ki-1 lymphoma (Mac-1) suppresses IL-2-dependent mitosis; however, the suppression is less than 45%. Paper-5796256.
Although normal control B-LCL express high-affinity IL-2 binding sites (Kd = 60 pM, 150 sites/cell), B-LCL derived from SCIDX1 patients failed to bind IL-2 under high-affinity conditions. Paper-111293.
In a nonhematological model, the P-gp expressing HCT-8 adenocarcinoma cell line, exogenously added IL-2 was shown to exert an inhibitory effect on P-gp mediated Rhodamine-123 efflux. Paper-661406.
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.
The combination signals of anti-CD3 MoAb and either IL-2 or IL-4 produced a proliferative response greater than anti-CD3 MoAb alone ( P less than .01) or lymphokine alone ( P less than .01). Paper-6920598.
HIV-1 gp160 as a modifier of Th1 and Th2 cytokine response: gp160 suppresses interferon-gamma and interleukin-2 production concomitantly with enhanced interleukin-4 production in vitro. Paper-134536.
Instead, IL-2-receptor interactions actually promote the loss of IL-2 responsiveness by diminishing the density of high-affinity binding sites at the time that Tac antigen levels are increased. Paper-5050017.
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.
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 observed that concentrations of GM-CSF between 0.01 ng/mL and 10 ng/mL had a synergistic effect with concentrations of IL-2 between 1 U/mL and 10 U/mL in stimulating T-cell proliferation. Paper-113721.
Using phosphoamino acid analysis, JAK3 and STAT5 were determined to be serine and tyrosine- phosphorylated in response to IL-2 stimulation of the human natural killer-like cell line, YT. Paper-14228943.
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.
These experiments demonstrate that, after initial acquisition of the IL-2-R, IL-2 as well as antigen is able to directly upregulate both the level of IL-2-R mRNA and cell surface IL-2-R molecules. Paper-4868500.
CONCLUSION: Administration of IL-2/RA to this patient population produced a significant decrease in VEGF, improvement of prognostically relevant immunological parameters, and durable response in 25% of patients. Paper-13691745.
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.
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.
In addition, the induction of GAPDH is directly due to the effect of IL2, and not in conjunction with any serum components, since IL2 will induce GAPDH mRNA under serum-free conditions. Paper-6532053.
Leukemic cells from a chronic T-lymphocytic leukemia patient proliferated in response to both interleukin-2 and interleukin-4 without prior stimulation and produced interleukin-2 mRNA with stimulation. Paper-6025523.
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.
This reduced IL2R alpha expression on T-TIL was not responsible for the proliferative unresponsiveness since T-TIL that expressed both IL2R alpha and/or IL2R beta still failed to respond to high doses of IL2. Paper-7674801.
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.
It was found that IL-2 induced proliferative responses of PBL from IFN-alpha non-responders, collected prior to IFN-alpha therapy, were significantly decreased as compared to those from normal blood donors. Paper-980539.
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.
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.
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.
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.
In each patient, one tumor received 1 ml (50,000 IU) IFN alone or alternatively associated with 1 ml IL-2 twice a week for 4-6 weeks; another nodule situated 10-12 cm away was considered as a control and remained uninjected. Paper-7432326.
Before vaccination with SRL172 patients had a low proportion of PBMC producing IFNgamma and IL2 (all 10) and a higher proportion secreting IL4 (all three tested), suggesting a predominantly Th2 cytokine profile. Paper-1634652.
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.
Moreover, following IL-2 stimulation of T cells, SOCS-3 was able to interact with the IL-2 receptor complex, and in particular tyrosine phosphorylated Jak1 and IL-2Rbeta. Paper-1908920.
Systemic lupus erythematosus (SLE) T cells express high levels of cAMP response element modulator ( CREM) that binds to the IL-2 promoter and represses the transcription of the IL-2 gene. Paper-10776182.
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.
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.
In the current study, tunIL1 was shown to enchance L929 fibroblast proliferation, induce IL-2 secretion from human mononuclear cells and enhance IL-2 receptor expression by EL-4 murine lymphoma cells. Paper-827167.
BACKGROUND: The proto-oncogene product c-Rel is a Rel/NF-kappaB family transcription factor that plays a critical role in lymphoid cell development and mediates CD28- induced expression of interleukin 2 ( IL-2). Paper-8958913.
Transforming growth factor beta and cyclosporin A inhibit the inducible activity of the interleukin-2 gene in T cells through a noncanonical octamer-binding site. Paper-7568334.
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.
Unlike other SOCS family members, we find that SOCS2 can enhance interleukin-2 ( IL-2)- and IL-3-induced STAT phosphorylation following and potentiate proliferation in response to cytokine stimulation. Paper-10979446.
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.
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.
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.
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.
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.
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.
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.
CH925 is a novel fusion protein, being neither IL-6 nor IL-2, more potent than IL-2 and/or IL-6 and causing non- IL-2 and non-IL-6 functions of strong EPO-like and mild IL-3-like effects on erythroid progenitor cell growth. Paper-131278.
Five melanoma cell lines were transduced with IL-2- or IFN-gamma-containing vectors and secreted IL-2 at 1 to 40 U/mL/10(6) cells/24 h or IFN-gamma 1 to 8 U/mL/10(6) cells/24 h, respectively. Paper-7373847.
Together, these findings suggest that JAK3 is functionally important in activated monocytes and cells of the myeloid lineage and is involved in signaling responses of cytokines that use the common gamma-chain of the IL-2 receptor. Paper-189816.
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.
Functional expression of interleukin 2 receptor in a human factor-dependent megakaryoblastic leukemia cell line: evidence that granulocyte-macrophage colony-stimulating factor inhibits interleukin 2 binding to its receptor. Paper-7569322.
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.
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.
Phenotypic changes induced by interleukin-2 ( IL-2) and IL-3 in an immature T-lymphocytic leukemia are associated with regulated expression of IL-2 receptor beta chain and of protein tyrosine kinases LCK and LYN. Paper-7482842.
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.
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.
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.
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.
Other VV mutants that produced excess dsRNA also inhibited protein binding to the IL-2 enhancer, suggesting that the presence of viral dsRNA has a role in retaining NF-90 in the cytosol and regulating IL-2 gene expression. Paper-10134262.
Previous research has shown that shockwave treatment affects T-cell function, enhancing T-cell proliferation and IL-2 expression by activating p38 mitogen-activated protein kinase ( MAPK) signaling. Paper-14178513.
The treatment of CD4 T cells with HIV env or surface ligation of CD4 with anti-CD4 monoclonal antibodies inhibited the IL-2- induced activation of Jak-1 and Jak-3, as well as their targets, STAT5a and STAT5b. Paper-9876970.
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.
The results show that overexpression of ERK1 enhances expression of T-cell interleukin-2 ( IL-2), IL-3, and granulocyte-macrophage colony-stimulating factor mRNA; no change was seen in expression of the alpha-actin gene. Paper-102509.
Reversible protein phosphorylation plays a key role in interleukin-2 ( IL-2) receptor- mediated activation of Janus tyrosine kinase 3 ( JAK3) and signal transducer and activator of transcription 5 ( STAT5) in lymphocytes. Paper-14228943.
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.
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.
Janus kinase 3 ( JAK3) is a cytoplasmic tyrosine kinase required for T cell development and activated by cytokines that utilize the interleukin-2 ( IL-2) receptor common gamma chain (gamma(c)). Paper-1882359.
However, high concentrations of IL-2 strongly blocked IL-18-induced NK cell apoptosis through alleviating IL-18-induced FasL expression and activation of Fas-mediated death signaling and increasing anti-apoptosis molecule (Bcl-X(L)). Paper-15522608.
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.
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.
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.
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.
Addition of a specific TGF-beta 1 antibody reversed the inhibitory effect of some concentrates on IL-2 secretion by PHA- stimulated Jurkat T cells and interleukin-5 (IL-5)-induced proliferation of an erythroleukemic cell line. Paper-131771.
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.
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.
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.
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.
Plasma tumor necrosis factor-alpha ( TNF-alpha) levels, but not interferon-gamma ( IFN-gamma) levels, increased during IL-2 treatment, but spontaneous and IL-2- stimulated TNF-alpha secretion in vitro remained abnormally low. Paper-6829341.
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.
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.
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.
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.
These findings suggest that a significant cytotoxicity against tumor cells can be mediated by eosinophils after indirect, IL-5- mediated in vivo activation by IL-2, and that eosinophils may be involved in the anti-tumor response(s) induced in vivo by IL-2. Paper-7888385.
NFAT 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. Paper-15351482.
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.
The ability of these mutated IL-2R gamma chains to participate in the function of a high-affinity IL-2R complex was examined by radiolabeled IL-2 binding studies using Epstein-Barr virus-transformed B lymphoblastoid cell lines (B-LCL) derived from SCIDX1 patients. Paper-111293.
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.
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.
The following changes reached significance (p <.05): prolactin (versus prolactin antibody) increased tumor necrosis factor-alpha ( TNF-alpha) and interferon-gamma ( IFN-gamma) producing CD4+ and CD8+ cells and interleukin-2 ( IL-2) producing CD8+ cells. Paper-10446487.
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.
We also found that wild-type CD26 ( DPPIV+) transfectants produced more IL-2 than mutant CD26 (DPPIV-)-transfected cells or CD26- control transfectants when triggered by stimuli not involving CD26, such as anti-CD3 and phorbol ester. Paper-91664.
These findings indicate that induction of FOXP3 is intrinsic to CD8 T cells that are activated in the presence of IL-2 or IL-15, and in vitro-induced expression of FOXP3 cannot be simply interpreted as an indicator of Treg activity or activation marker. Paper-13168827.
Up to 79% of naive CD4(+) T cells (median, 61%) from patients in the IL-2 group expressed CD25, and the number of naive CD4(+)/CD25(+) T cells correlated positively with both the total and naive CD4(+) T-cell counts. Paper-9540975.
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.
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.
These studies indicate that the HLA- beta 2m class I antigen complex plays a role in T lymphocyte activation via release of IL 2, and suggest the existence of different mechanisms for activation of IL 2 producers and IL 2 responders in 1 degree MLC. Paper-5133017.
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.
We show in this study that the inhibitory action of TGF-beta on T lymphocytes is accompanied by a block of interleukin 2 ( IL-2) gene expression which is mediated, at least in part, by inhibition of IL-2 promoter/enhancer activity. Paper-7568334.
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.
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.
However, the same monoclonal antibody failed to reduce IL-6-driven thymocyte proliferation in the presence of a suboptimal PHA concentration, suggesting that IL-6 stimulates thymocyte proliferation by way of IL-2-dependent and IL-2-independent pathways. Paper-6008740.
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.
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.
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.
Although the mechanisms governing IL-2- induced tyrosine phosphorylation and activation of JAK3/ STAT5 have been extensively studied, the role of serine/ threonine phosphorylation in controlling these effectors remains to be elucidated. Paper-14228943.
The following parameters were studied: 1) Effect of HBV-IC (HBsAg-IgG or HBeAg-IgG) on PHA-mediated lymphocyte proliferation; 2) Influence of HBV-IC on the ability of PHA- stimulated peripheral blood lymphocytes (PBL) for IL-2 production and IL-2 receptor expression. Paper-6676249.
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.
Experiments performed with the IL-2-dependent murine CTLL-2 cell line and with PHA- stimulated human peripheral blood mononuclear cells showed that the purified sIL-2R at concentrations up to about 300 nM was unable to block IL-2-dependent cell proliferation. Paper-7332813.
In the current study, we demonstrated that the winged-helix transcription factor IL-2 enhancer binding factor ( ILF) is constitutively expressed in both resting and activated Jurkat cells and binds to two adjacent sequence motifs immediately downstream of the binding site for NFAT. Paper-952078.
The fact that proliferative unresponsiveness exists even though T-TIL can produce IL2 and express IL2R alpha/beta suggests that T-TIL have a selective loss of a common intracellular signaling pathway which is requisite to proliferation but not other aspects of response to antigenic stimulation. Paper-7674801.
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.
Tumor necrosis factor alpha ( TNF alpha) enhanced the IL-2-dependent proliferation of TIL's cultured in low concentrations of IL-2 (10 U/ml); however, neither TNF alpha nor interferon gamma was able to reduce the inhibitory effect of TGF beta 2 on TIL proliferation. Paper-6478503.
Inhibition of AMPK by compound C, a specific inhibitor of AMPK or small interfering RNA of AMPKalpha1 suppressed IL-2 production in Jurkat T cells and peripheral blood lymphocytes stimulated with PMA plus ionomycin (PMA/Io) or with monoclonal anti-CD3 plus anti-CD28. Paper-14714266.
CONCLUSION: The observation that IL15 can restore the function of WT1-specific T cells that were unresponsive to IL2 has implications for vaccination and immunotherapeutic strategies that aim to enhance WT1-specific T cell immunity in patients. Paper-13638367.
The LAK activity induced by human recombinant IL-2 was very similar in controls and patients with rheumatoid arthritis but was significantly decreased in patients with sarcoidosis, although the frequency of LAK-cell precursors measured using a limiting dilution assay was comparable in all three groups. Paper-5489221.
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.
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.
In vivo and in vitro production of tumor cytotoxic cytokines tumor necrosis factor-alpha ( TNF-alpha) and interferon-gamma ( IFN-gamma) was significantly stimulated following IL-2 therapy, further indicating IL-2-mediated stimulation of the antineoplastic activity of the immune system. Paper-134000.
We now report that PA682BM-1 can be triggered by the protein kinase C (PKC) activators, phorbol 12-myristate 13-acetate (PMA) and (-) Indolactam-v, to secrete IFN gamma, whereas JLP(c) cells spontaneously produce low levels of IFN gamma that can be enhanced by PKC activators and interleukin-2 ( IL-2). Paper-7482112.
T cells grown in response to CD3 plus CD28 plus IL-2 stimulation produced both IL-4 and interferon-gamma ( IFN-gamma) on restimulation (Th0 cells) and could be functionally differentiated into Th1- or Th2-type cells by the addition of IFN-gamma or IL-4, respectively, during cell cloning. Paper-571513.
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.
These results suggest that CN is involved in the coordinated induction of the GM-CSF and IL-2 genes and that the CLE0 sequence of the GM-CSF gene is a functional analogue of the NF-AT- binding site in the IL-2 promoter, which mediates signals downstream of T cell activation. Paper-120808.
In a human granulocyte-macrophage colony-stimulating factor ( GM-CSF), IL-3, or stem cell factor-dependent myeloid leukemia cell line (M07E), IL-2 was found to stimulate proliferation in a dose-dependent manner and to augment GM-CSF- and stem cell factor-induced proliferation of M07E cells. Paper-7569322.
This study explores the use of a liver-specific albumin promoter and a tumor-specific alpha-fetoprotein ( AFP) enhancer to achieve the regulated expression of the cytokine interleukin-2/interferon alpha2b ( IL-2/IFNalpha2b) fused gene for treatment of hepatocellular carcinoma ( HCC). Paper-1792134.
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.
In this study, a comparison of draining lymph node cells from L. amazonensis- and L. major-infected mice at 10 weeks postinfection showed equivalent percentages of effector/memory phenotype CD44hi CD4+ T cells producing interleukin-2 ( IL-2) and proliferating after antigen stimulation. Paper-11363564.
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.
Our studies show that the mechanism of IL-10 regulation of quiescent CD4(+) T-cell activation is mainly by blocking induction of IL-2 that is critical to downregulation of p27(Kip1) and upregulation of D cyclins in T-cell activation and entry into the cell cycle. Paper-1705894.
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.
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.
These studies indicate that the CD28- regulated signal transduction pathway is activated during SE stimulation of T cells and plays an important role in SE induction of IL-2 gene expression through its influence upon the CD28-responsive element contained within the IL-2 gene promoter. Paper-55961.
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.
Here, we demonstrate that interleukin-2 ( IL-2) induces FOXP3 expression in OKT3-stimulated or antigen-stimulated CD8 T cells, indicating that FOXP3 expression is neither limited to a unique subset of CD8 T cells nor dependent on the mode of T-cell receptor stimulation. Paper-13168827.
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 mixture of rabbit antibodies specific for recombinant interleukin-1 alpha ( IL-1 alpha) and interleukin-1 beta ( IL-1 beta) inhibited Schwann cell proliferation induced by unfractionated human cytokines whereas antibodies to interleukin-2 ( IL-2) and control IgG did not. Paper-6869686.
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.
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.
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.
We report here the detection of four new alleles designated IL-2 A* (122 bp), IL-2R-2 (169 bp), IL-2R 0 (165 bp), and IL-2R 9 (147 bp) in patients with rheumatoid arthritis and normal controls from the Pacific Northwest. The number of alleles now recognized at these loci within the IL-2 and IL-2Rbeta genes increases to 16 and 12, respectively. Paper-8780130.
Notably, the cells infected with the bFGF- expressing adenovirus containing the IL-2 signal sequence were markedly enhanced cell survival in the early phase of the culture, compared with the control cells and even those infected with the bFGF- expressing adenovirus without the IL-2 signal sequence. Paper-8519478.
Although the expression of IL-2R beta was not down-regulated but somewhat up-regulated by treatment with GM-CSF in both mRNA and protein levels, GM-CSF was found to compete (75%) with radiolabeled IL-2 for binding to IL-2R on M07E cells, whereas no competition of GM-CSF binding was observed with IL-2 even at a 400-fold molar excess. Paper-7569322.
The differential propensity of CD8(+) T cells to produce either IL-2 or perforin is in part related to levels of CD28 and the transcription factor T-bet, as CD8(+) T cells that rapidly upregulate perforin harbor high levels of T-bet and those producing IL-2 express high amounts of CD28. Paper-14272655.
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.
Expression of the full-length complementary DNA encoding NF-ATc activates the interleukin ( IL-2) promoter in non-T lymphocytes, whereas a dominant negative of NF-ATc specifically blocks activation of the IL-2 promoter in T lymphocytes, indicating that NF-ATc is required for IL-2 gene expression. Paper-122216.
We report that virus-specific CD4+ T cells expressing 4-1BB ( CD137) or OX40 ( CD134) produced more IL-2 than cells lacking these costimulatory receptors (P<0.05) and that 4-1BB was expressed at a lower level on HIV- than CMV-specific IFN-gamma and IL-2 producing CD4+ T cells (P<0.0001 and P<0.01, respectively). Paper-13885630.
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.
In the present study, we examined function of a mutant gammac chain (A156V) isolated from an X-SCID patient and found that T cells expressing the mutant gammac chain were selectively impaired in their responses to IL-4 or IL-7 compared with the wild-type gammac chain expressing cells although responses to IL-2 or IL-15 were relatively maintained. Paper-1795499.
In this paper, we provide evidence that IL-2- mediated induction of the c-myb gene occurs via the phosphoinositide 3-kinase ( PI3K) signaling pathway, that protein kinase B ( PKB) is the principal transducer of this signal, and that activation of the c-myb promoter can be abolished by deletion of conserved E2F and NF-kappaB binding sites. Paper-9037613.
In this study, we observed that IL-18 induced NK cell apoptosis and inhibited NK cell expansion in the presence of low concentrations of interleukin-2 ( IL-2), while high concentrations of IL-2 overcame these effects of IL-18, and high concentrations of IL-2 promoted the stimulatory activity of IL-18 on NK cells. Paper-15522608.
Immunomodulatory drugs (IMiDs) are orally available small molecules that potently inhibit tumor necrosis factor-alpha ( TNF-alpha) production by lipopolysaccharide (LPS)- stimulated human peripheral blood mononuclear cells (HuPBMCs) but enhance secretion of such cytokines as interleukin-2 ( IL-2) and interferon-gamma ( IFN-gamma) by stimulated T cells. Paper-11248933.
Suppression of viral replication with antiretroviral therapy was associated with increased 4-1BB expression on HIV- and CMV-specific IL-2 producing CD4+ T cells (P<0.05 and P<0.01, respectively) and the percentage of IL-2 producing HIV-specific CD4+ T cells that expressed 4-1BB was inversely correlated with HIV plasma viral load (r=-0.75, P=0.007). Paper-13885630.
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: V00564 (NCBI_GENBANK__AC), Q9C001 (UNIPROT__AC), P01585 (UNIPROT__AC), BC066256 (NCBI_GENBANK__AC).
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 Bos taurus.
IL2 is a homologue of Il2 (interleukin 2) from Mus musculus.
IL2 is a homologue of Il2 (interleukin 2) from Rattus norvegicus.
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iHOP - Information Hyperlinked over Proteins .
Concept & Implementation by Robert Hoffmann.