Experimental autoimmune encephalomyelitis is a CD4+ T cell–mediated demyelinating disease of the CNS that serves as a model for multiple sclerosis. Cytokines and chemokines shape Th1 and Th17 effector responses as well as regulate migration of leukocytes to the CNS during disease. The CNS cellular infiltrate consists of Ag-specific and nonspecific CD4+ and CD8+ T cells, neutrophils, B cells, monocytes, macrophages, and dendritic cells. The mechanism of immune-mediated inflammation in experimental autoimmune encephalomyelitis has been extensively studied in an effort to develop therapeutic modalities for multiple sclerosis and, indeed, has provided insight in modern drug discovery. The present Brief Review highlights critical pathogenic aspects of cytokines and chemokines involved in generation of effector T cell responses and migration of inflammatory cells to the CNS. Select cytokines and chemokines are certainly important in the regulatory response, which involves T regulatory, B regulatory, and myeloid-derived suppressor cells. However, that discussion is beyond the scope of this brief review.

中文翻译：

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实验性自身免疫性脑脊髓炎发病机制中的细胞因子和趋化因子

实验性自身免疫性脑脊髓炎是一种 CD4+ T 细胞介导的中枢神经系统脱髓鞘疾病，可作为多发性硬化症的模型。细胞因子和趋化因子塑造 Th1 和 Th17 效应反应，并在疾病期间调节白细胞向 CNS 的迁移。CNS 细胞浸润由 Ag 特异性和非特异性 CD4+ 和 CD8+ T 细胞、中性粒细胞、B 细胞、单核细胞、巨噬细胞和树突细胞组成。实验性自身免疫性脑脊髓炎中免疫介导炎症的机制已被广泛研究，以开发多发性硬化症的治疗方式，并且确实为现代药物发现提供了见解。本简要综述重点介绍了与效应 T 细胞反应的产生和炎症细胞向中枢神经系统迁移有关的细胞因子和趋化因子的关键致病方面。选择细胞因子和趋化因子在调节反应中当然很重要，这涉及 T 调节、B 调节和髓源性抑制细胞。但是，该讨论超出了本简要回顾的范围。