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首页> 外文期刊>Cytokine >Cyclosporin A inhibits the production of IL-17 by memory Th17 cells from healthy individuals and patients with rheumatoid arthritis.
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Cyclosporin A inhibits the production of IL-17 by memory Th17 cells from healthy individuals and patients with rheumatoid arthritis.

机译：环孢菌素A抑制健康个体和类风湿关节炎患者的记忆Th17细胞产生IL-17。

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摘要

Recent evidence from several studies indicated that IL-17-producing Th17 cells can represent the key effector cells in the induction and development of autoimmune disorders. Cyclosporine A (CsA) is a commonly used immunosuppressant to treat lots of autoimmune diseases including rheumatoid arthritis (RA). Here, we demonstrated that PBMCs and purified CD4(+) T cells from healthy individuals and patients with RA could be induced to produce large amounts of IL-17 after stimulation with anti-CD3 plus anti-CD28 mAbs. Phenotypic analysis indicated that the majority of IL-17-producing cells were Th17 cells with memory phenotype. The addition of CsA into cell cultures significantly inhibited the IL-17 production by Th17 cells at protein and at mRNA levels. Compared to the PBMCs from normal individuals, PBMCs from the patients with RA produced higher levels of IL-17 that was also significantly inhibited by CsA both at protein and at mRNA levels. The mechanism might be the effect of CsA on the T cells activation because the expression of CD69 and CD25 molecules on T cells was markedly reduced in the presence of CsA. Taken together, these results demonstrated that CsA suppressed the IL-17 production and inhibited the Th17 cells differentiation from both healthy individuals and patients with RA.
机译：来自几项研究的最新证据表明，产生IL-17的Th17细胞可以代表自身免疫疾病的诱导和发展过程中的关键效应细胞。环孢霉素A（CsA）是一种常用的免疫抑制剂，可用于治疗许多自身免疫疾病，包括类风湿关节炎（RA）。在这里，我们证明了用抗CD3加抗CD28 mAb刺激后，健康人和RA患者的PBMC和纯化的CD4（+）T细胞可被诱导产生大量IL-17。表型分析表明，大多数产生IL-17的细胞是具有记忆表型的Th17细胞。在细胞培养物中加入CsA可以显着抑制Th17细胞在蛋白质和mRNA水平上产生IL-17。与正常人的PBMC相比，RA患者的PBMC产生更高水平的IL-17，在蛋白质和mRNA水平，IL-17也被CsA显着抑制。该机制可能是CsA对T细胞活化的影响，因为在存在CsA的情况下，T细胞上CD69和CD25分子的表达显着降低。综上，这些结果表明，CsA抑制了IL-17的产生，并抑制了健康人和RA患者的Th17细胞分化。

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