Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P14784 (IL-2 receptor)
 3,849 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Influences of methionine enkephalin (met-enk) on delayed hypersensitivity (DH) against 2,4-dinitrofluoro-benzene (DNFB) and interleukin-2 (IL-2) production of mouse lymphocytes were examined. Met-enk enhanced the DH response to ear challenge when mice were treated with met-enk beginning at the same time as cpicutaneous sensitization with DNFB but not after being sensitized. When met-enk (10 nmol.L-1-100 mumol.L-1) was included in Con A-stimulated lymphocyte cultures, the IL-2 production increased in a concentration-dependent manner. Furthermore, in vivo treatment with met-enk also increased IL-2 production of splenocytes, and the enhancement of IL-2 production was parallel to that of lymphocyte proliferation. However, met-enk 10 nmol.L-1 had no effect on IL-2 receptor expression on thymocytes, splenocytes, and gut-associated lymphocytes. The data suggested that the stimulative effect of met-enk on lymphocytes may be mediated through the increase of IL-2, but not through the IL-2 receptor expression.
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PMID:Influence of methionine-enkephalin on interleukin-2 production and interleukin-2 receptor expression. 159 29

Cigarette smoking has been shown to cause profound suppression of T-cell responses in the lungs, but the mechanism by which this phenomenon occurs is not known. We have shown that 10 microM p-benzoquinone (p-BQ), a thiol-reactive benzene derivative found in cigarette tar, inhibits mitogen-induced IL-2 production by human peripheral blood mononuclear cells by 76 +/- 7% without affecting lymphocyte/macrophage agglutination or blast transformation. The effect of p-BQ appeared to be specific for IL-2 production, since de novo induction of the IL-2 receptor alpha-chain (CD25) and ICAM-1 (CD54) and upregulation of LFA-1 alpha/beta (CD11a and CD18) were unaffected. In contrast, N-ethylmaleimide (NEM), another alpha,beta-unsaturated diketone with thiol-reactive properties similar to those of p-BQ, inhibited all of these Con A-induced activation events. These results suggest that p-BQ inhibits T-cell mitogenesis by blocking a thiol-dependent event that controls IL-2 production but not other T-cell activation events.
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PMID:The cigarette tar component p-benzoquinone blocks T-lymphocyte activation by inhibiting interleukin-2 production, but not CD25, ICAM-1, or LFA-1 expression. 907 89

Hydroquinone (HQ), a reactive metabolite of benzene, is present in cigarette smoke and is known to inhibit mitogen-stimulated activation of both T and B lymphocytes. Despite extensive study, the underlying mechanism for HQ's immunotoxicity is not clear. NF-kappa B is a transcription factor known to regulate the expression of a number of genes critical for normal T cell activation. We therefore hypothesized that NF-kappa B might be involved in HQ-induced immunosuppression. In this study, we demonstrate that 1 microM HQ inhibits tumor necrosis factor alpha induced activation of NF-kappa B in primary human CD4+ T cells. This inhibition is not accompanied by a loss in viability, and HQ-treated T cells maintain other active signaling pathways throughout the exposure duration. Additionally, the inhibition of NF-kappa B is reversible as HQ-treated T cells regain normal functioning after 72 h in culture. HQ does not appear to alter NF-kappa B directly as preincubation of nuclear extracts with HQ does not diminish activity of this protein. We further demonstrate that 1 microM HQ inhibits intracellular IL-2 production in T cells stimulated with phorbol ester but does not alter surface expression of CD25 (the alpha-subunit of the IL-2 receptor). These data suggest that NF-kappa B may be an important molecular mediator of HQ's (and benzene's) immunotoxicity.
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PMID:Hydroquinone, a reactive metabolite of benzene, inhibits NF-kappa B in primary human CD4+ T lymphocytes. 957 86