Non-genomic rapid inhibition of Na +/H +-exchange 1 and apoptotic immunosuppression in human T cells by glucocorticoids

ChangC.-P.; WangS.-W.; HuangZ.-L.WangO.Y.-H.HuangM.I.-T.LuL.-M.TarngD.-C.ChienC.-H.ChienE.J.

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Non-genomic rapid inhibition of Na +/H +-exchange 1 and apoptotic immunosuppression in human T cells by glucocorticoids

机译：Non-genomic快速抑制Na + / H +交换在人类T 1和凋亡免疫抑制细胞通过糖皮质激素

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Glucocorticoids (GCs) have been employed as immunosuppressive agents for many years. However, it is still unclear how GCs instantly uncouple T cells from acute stressful inflammatory. In terms of time scale, the genomic activity of the classic GC receptor cannot fulfill this role under crisis; but a rapid non-genomic response can. In a previous study, intracellular acidification was found to be due to a rapid non-genomic inhibition of Na +/H +-exchange 1 (NHE1) and this event led to the immunosuppression of T cell proliferation by progesterone. The aim of this study was to examine whether there is a rapid acidification response caused by an inhibition of NHE1 activity and to explore the differential non-genomic effect on immunosuppression of hydrocortisone and dexamethasone. The IC 50 values for NHE1-dependent pH i recovery by hydrocortisone and dexamethasone are 250 and 1 nM, respectively. Co-stimulation of GCs with phytohemagglutinin (PHA) is able to inhibit PHA-induced IL-2 secretion, IL-4 secretion, and T-cell proliferation. Furthermore, apoptosis in PHA-activated T cells is not induced by hydrocortisone but by dexamethasone. The mechanism of immunosuppression on proliferation by dexamethasone was found to be different of hydrocortisone and seems to involve cytotoxicity against T cells. Moreover, apoptosis induced by dexamethasone and impermeable dexamethasone - bovine serum albumin suggests that the apoptotic immunosuppression occurs through both the plasma membrane and cytoplasmic sites. The rapid inhibitory responses triggered by GCs would seem to release T cells instantly when an acute stress-related response is needed. Nonetheless, the apoptotic immunosuppression by dexamethasone is attributable to its severe cytotoxicity.

机译：糖皮质激素(gc)工作免疫抑制药物多年。目前还不清楚如何GCs立即解开T急性压力的炎性细胞。时间尺度的基因活动经典的GC受体不能履行这个角色在危机;可以。酸化由于迅速被发现non-genomic抑制Na + / H +交换1(NHE1)和这个事件导致的免疫抑制T细胞增殖孕激素。检查是否有快速酸化NHE1活动的反应造成的抑制作用并探讨微分non-genomic影响氢化可的松和免疫抑制地塞米松。氢化可的松NHE1-dependent pH值我复苏分别和地塞米松是250和1海里。Co-stimulation GCs植物凝集素(PHA)能够抑制PHA-induced - 2分泌,分泌il - 4和t细胞扩散。PHA-activated不诱导T细胞氢化可的松,而是地塞米松。免疫抑制细胞增殖的机制地塞米松是不同的氢化可的松,似乎涉及细胞毒性对T细胞。地塞米松和不透水地塞米松-牛血清白蛋白表明凋亡通过等离子体发生免疫抑制膜和细胞质网站。抑制反应GCs似乎引发了急性时立即释放T细胞与压力相关的响应是必要的。地塞米松的凋亡免疫抑制由于其严重的细胞毒性。

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来源
《Journal of Cellular Physiology》 |2010年第3期|679-686|共8页
作者
ChangC.-P.; WangS.-W.; HuangZ.-L.WangO.Y.-H.HuangM.I.-T.LuL.-M.TarngD.-C.ChienC.-H.ChienE.J.;
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作者单位

Department of Physiology and Pharmacology, Chang-Gung University, Taoyuan, Taiwan;

Institute of Physiology, School of Medicine, National Yang-Ming University, Beitou, Taipei 11221;

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正文语种英语
中图分类细胞生物学;
关键词
T-Lymphocytes; Acquired Immunodeficiency Syndrome; T-Cell ProliferationPlasma membraneImmunosuppressionGlucocorticoidsHydrocortisoneImmunosuppressive Agents;

机译：t淋巴球;获得性免疫缺陷综合征;t细胞ProliferationPlasma;

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Non-genomic rapid inhibition of Na +/H +-exchange 1 and apoptotic immunosuppression in human T cells by glucocorticoids

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