Disequilibrium of T helper type 1, 2 and 17 cells and regulatory T cells during the development of experimental autoimmune myasthenia gravis
Disequilibrium of T helper type 1, 2 and 17 cells and regulatory T cells during the development of experimental autoimmune myasthenia gravis
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实验性自身免疫性重症肌无力发展过程中辅助性 T 细胞 1、2 和 17 型与调节性 T 细胞的不平衡
DOI：
10.1111/j.1365-2567.2009.03089.x
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发表时间：
2009-09-01
期刊：
影响因子：
6.4
通讯作者：
Li, Hulun
中科院分区：
文献类型：
--
作者：
Mu, Lili;Sun, Bo;Li, Hulun
实验性自身免疫性重症肌无力（Experimental autoimmune myasthenia gravis，EAMG）是一种以自身抗原烟碱乙酰胆碱受体（nicotinic acetylcholine receptor，AChR）为靶点的罕见器官特异性自身免疫性疾病。我们发现在EAMG的发展过程中，辅助性T细胞1型（Th 1）、Th 2、Th 17和调节性T细胞（Treg）亚群的平衡发生了重新分布，白细胞介素-17（IL-17）细胞因子参与了EAMG的发生。Th 17细胞的比例随着疾病进展而变化最显著，伴随着IL-17水平的上调。此外，AChR肽特异性T细胞和抗AChR抗体分泌细胞的增殖能力在体外被IL-17刺激时增加。提示EAMG患者外周血中CD 4+辅助性T细胞亚群的失衡促进了EAMG的发生发展，Th 17细胞通过分泌IL-17介导自身免疫反应的致病机制为重症肌无力的治疗提供了新的靶点。
P>Experimental autoimmune myasthenia gravis (EAMG), an animal model of myasthenia gravis (MG), is a rare organ-specific autoimmune disease targeting the autoantigen nicotinic acetylcholine receptor (AChR). We show here that the balance of T helper type 1 (Th1), Th2, Th17 and regulatory T (Treg) subsets of CD4(+) helper T cells were redistributed during the development of EAMG and that the interleukin-17 (IL-17) cytokine is involved in this disease. The ratio of Th17 cells changed most notably with disease progression accompanied by an up-regulated level of IL-17. Moreover, the proliferative ability of AChR peptide-specific T cells and the anti-AChR antibody-secreting cells increased when stimulated by IL-17 in vitro. These findings suggested that the disequilibrium of the CD4(+) helper T-cell subsets could promote the development of EAMG, and the pathogenic mechanism by which Th17 cells drives autoimmune responses by secreting cytokine IL-17 provides a new target for myasthenia gravis therapy.