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17-beta-estradiol suppresses IL-2 and IL-2 receptor.

机译:17-β-雌二醇抑制IL-2和IL-2受体。

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Interleukin-2 (IL-2) plays an important role in adaptive immune responses. These responses differ between females and males and may be due to the sex steroid estrogen. In this investigation we show that estrogen suppresses IL-2 production from activated peripheral blood T cells and CD4+ T cell lines at the transcriptional level. Suppression of IL-2 occurred at short term, high 17-beta-estradiol concentrations as well as longer term lower 17-beta-estradiol concentrations. In CD4+ Jurkat T cells, suppression of IL-2 was associated with decreased nuclear binding of two important IL-2 promoter transcription factors: NFkappaB and AP-1. The decreased nuclear binding of NFkappaB occurred in the setting of estrogen-induced increases in IkappaBalpha protein levels, an important inhibitor of NFkappaB nuclear translocation. 17-beta-Estradiol was also shown to inhibit IL-2 receptor (IL-2R) expression in activated peripheral blood T cells. Estrogen-induced suppression of IL-2 and its receptor may have many ramifications for our understanding of immune and autoimmune sexual dichotomies, immune responses during pregnancy, and potential therapeutic intervention with hormone agonists and antagonists. Copyright 2001 Academic Press.
机译:白介素2(IL-2)在适应性免疫应答中起着重要作用。这些反应在女性和男性之间有所不同,可能是由于性类固醇雌激素所致。在这项研究中,我们表明雌激素在转录水平上抑制了活化的外周血T细胞和CD4 + T细胞系产生IL-2。 IL-2的抑制作用发生在短期,高17-β-雌二醇浓度以及长期较低的17-β-雌二醇浓度。在CD4 + Jurkat T细胞中,IL-2的抑制与两个重要IL-2启动子转录因子NFkappaB和AP-1的核结合减少有关。 NFkappaB核结合的减少发生在雌激素诱导的IkappaBalpha蛋白水平升高的背景下,这是NFkappaB核易位的重要抑制剂。还显示17-β-雌二醇可抑制活化的外周血T细胞中的IL-2受体(IL-2R)表达。雌激素诱导的IL-2及其受体的抑制作用可能对我们对免疫和自身免疫性二分法,怀孕期间的免疫反应以及激素激动剂和拮抗剂的潜在治疗干预的理解有很多影响。版权所有2001,学术出版社。

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