17-β-estradiol suppresses IL-2 and IL-2 receptor
17-β-estradiol suppresses IL-2 and IL-2 receptor
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DOI：
10.1006/cyto.2001.0900
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发表时间：
2001-06-21
期刊：
影响因子：
3.8
通讯作者：
Jenkins, JK
中科院分区：
文献类型：
--
作者：
McMurray, RW;Ndebele, K;Jenkins, JK
白细胞介素-2（IL-2）在获得性免疫应答中起重要作用。这些反应在女性和男性之间不同，可能是由于性类固醇雌激素。在这项研究中，我们表明，雌激素抑制IL-2的生产从活化的外周血T细胞和CD 4 + T细胞系在转录水平。IL-2的抑制发生在短期、高17-β-雌二醇浓度以及长期较低的17-β-雌二醇浓度下。在CD 4 + Jurkat T细胞中，IL-2的抑制与两个重要的IL-2启动子转录因子NF kappaB和AP-1的核结合减少相关。NF κ B的核结合减少发生在雌激素诱导的I κ B α蛋白水平增加的情况下，I κ B α蛋白水平是NF κ B核转位的重要抑制剂。17-β-雌二醇还显示抑制活化的外周血T细胞中的IL-2受体（IL-2 R）表达。雌激素诱导的IL-2及其受体的抑制可能对我们理解免疫和自身免疫性二分法、妊娠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有许多影响。(C)北京：科学出版社.
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: NF kappaB and AP-1. The decreased nuclear binding of NF kappaB occurred in the setting of estrogen-induced increases in I kappaB alpha protein levels, an important inhibitor of NF kappaB 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. (C) 2001 Academic Press.