CCL2 recruitment of IL-6-producing CD11b+ monocytes to the draining lymph nodes during the initiation of Th17-dependent B cell-mediated autoimmunity
CCL2 recruitment of IL-6-producing CD11b+ monocytes to the draining lymph nodes during the initiation of Th17-dependent B cell-mediated autoimmunity
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在 Th17 依赖性 B 细胞介导的自身免疫启动过程中，CCL2 将产生 IL-6 的 CD11b 单核细胞募集至引流淋巴结
DOI：
10.1002/eji.200737973
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发表时间：
2008-07-01
影响因子：
5.4
通讯作者：
Shi, Fu-Dong
中科院分区：
文献类型：
--
作者：
Bai, Ying;Liu, Ruolan;Shi, Fu-Dong
Th17 细胞的发育和功能部分受到细胞因子 TGF-P、IL-23 和 IL-6 的影响，但在自身免疫启动过程中控制 Th17 细胞招募和活性的机制仍不清楚。我们在此表明，实验性自身免疫性重症肌无力（人类重症肌无力的动物模型）次级淋巴器官中自身反应性 Th17 细胞的发育是由产生 IL-6 的 CD11b(+) 细胞通过 CC 趋化因子配体 2 (CCL2) 调节的。值得注意的是，乙酰胆碱受体 (AChR) 反应性 Th17 细胞帮助 B 细胞产生抗 AChR 抗体，这些抗体会导致神经肌肉传递受损，从而导致自身免疫的临床表现，IL-17 缺陷小鼠中缺乏疾病诱导就表明了这一点。因此，Th17 细胞可以通过涉及 CCL2 的新机制促进体液自身免疫。
The development and function of Th17 cells are influenced in part by the cytokines TGF-P, IL-23 and IL-6, but the mechanisms that govern recruitment and activity of Th17 cells during initiation of autoirnmunity remain poorly defined. We show here that the development of autoreactive Th17 cells in secondary lymphoid organs in experimental autoimmune myasthenia gravis - an animal model of human myasthenia gravis - is modulated by IL-6-producing CD11b(+) cells via the CC chemokine ligand 2 (CCL2). Notably, acetylcholine receptor (AChR)-reactive Th17 cells provide help for the B cells to produce anti-AChR antibodies, which are responsible for the impairment of the neuromuscular transmission that contributes to the clinical manifestations of autoirnmunity, as indicated by a lack of disease induction in IL-17-deficient mice. Thus, Th17 cells can promote humoral autoirnmunity via a novel mechanism that involves CCL2.