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Cyclosporin A inhibits the production of IL‐17 by memory Th17 cells from healthy individuals and patients with RA
Author(s) -
Wu Changyou,
Zhang Cai,
Yang Binyan
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1074.17
Subject(s) - peripheral blood mononuclear cell , cd28 , effector , stimulation , immunology , il 2 receptor , phenotype , cd3 , t cell , chemistry , biology , in vitro , medicine , endocrinology , immune system , cd8 , gene , biochemistry
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. Cyclosporin A (CsA) is a commonly used immunosuppressive agent to treat a wide range of autoimmune disorders including RA. Here, we demonstrate that PBMCs and purified CD4+ T cells from healthy individuals and patients with RA could be induced to produce a large amount 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 production of IL‐17 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 both at protein and at mRNA levels by CsA. The mechanism might be the effect of CsA on the activation of T cells 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 production of IL‐17 and inhibited the differentiation of Th17 cells from both healthy individuals and patients with RA.