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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >NLRP3 inflammasome induces chemotactic immune cell migration to the CNS in experimental autoimmune encephalomyelitis
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NLRP3 inflammasome induces chemotactic immune cell migration to the CNS in experimental autoimmune encephalomyelitis

机译：NLRP3炎性小体在实验性自身免疫性脑脊髓炎中诱导趋化性免疫细胞迁移至CNS

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摘要

The NLRP3 inflammasome is a multiprotein complex consisting of three kinds of proteins, NLRP3, ASC, and pro-caspase-1, and plays a role in sensing pathogens and danger signals in the innate immune system. The NLRP3 inflammasome is thought to be involved in the development of experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS). However, the mechanism by which the NLRP3 inflammasome induces EAE is not clear. In this study, we found that the NLRP3 inflammasome played a critical role in inducing T-helper cell migration into the CNS. To gain migratory ability, CD4~+ T cells need to be primed by NLRP3 inflammasome-sufficient antigen-presenting cells to up-regulate chemotaxis-related proteins, such as osteopontin, CCR2, and CXCR6. In the presence of the NLRP3 inflammasome, dendritic cells and macrophages also induce chemotactic ability and up-reg-ulate chemotaxis-related proteins, such as α4β1 integrin, CCL7, CCL8, and CXCL16. On the other hand, reduced Th17 cell population size in immunized Nlrp3~(-/-) and Ast~(-/-) mice is not a determinative factor for their resistance to EAE. As currently applied in clinical interventions of MS, targeting immune cell .migration molecules may be an effective approach in treating MS accompanied by NLRP3 inflammasome activation.
机译：NLRP3炎性小体是由三种蛋白质NLRP3，ASC和pro-caspase-1组成的多蛋白复合物，在先天免疫系统中检测病原体和危险信号时发挥作用。 NLRP3炎性小体被认为与实验性自身免疫性脑脊髓炎（EAE）的发展有关，EAE是多发性硬化症（MS）的动物模型。但是，NLRP3炎性体诱导EAE的机制尚不清楚。在这项研究中，我们发现NLRP3炎性小体在诱导T辅助细胞向CNS迁移中起关键作用。为了获得迁移能力，需要由NLRP3炎性小体充足的抗原呈递细胞启动CD4〜+ T细胞，以上调趋化相关蛋白，例如骨桥蛋白，CCR2和CXCR6。在存在NLRP3炎性体的情况下，树突状细胞和巨噬细胞还诱导趋化能力并上调趋化性相关蛋白，例如α4β1整联蛋白，CCL7，CCL8和CXCL16。另一方面，在免疫的Nlrp3（-/-）和Ast-（-/-）小鼠中，Th17细胞种群的减少并不是其对EAE耐药的决定性因素。如目前在MS的临床干预中所应用的，靶向免疫细胞迁移分子可能是治疗伴随NLRP3炎性体活化的MS的有效方法。

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