自身免疫
实验性自身免疫性脑脊髓炎
生物
脉络丛
效应器
免疫学
免疫系统
中枢神经系统
T细胞
神经科学
细胞生物学
作者
Federica Sallusto,Daniela Impellizzieri,Camilla Basso,Alice Laroni,Antonio Uccelli,Antonio Lanzavecchia,Britta Engelhardt
标识
DOI:10.1111/j.1600-065x.2012.01140.x
摘要
Summary: To perform their distinct effector functions, pathogen‐specific T cells have to migrate to target tissue where they recognize antigens and produce cytokines that elicit appropriate types of protective responses. Similarly, migration of pathogenic self‐reactive T cells to target organs is an essential step required for tissue‐specific autoimmunity. In this article, we review data from our laboratory as well as other laboratories that have established that effector function and migratory capacity are coordinately regulated in different T‐cell subsets. We then describe how pathogenic T cells can enter into intact or inflamed central nervous system (CNS) to cause experimental autoimmune encephalomyelitis or multiple sclerosis. In particular, we elaborate on the role of CCR6/CCL20 axis in migration through the choroid plexus and the involvement of this pathway in immune surveillance of and autoimmunity in the CNS.
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