Cytokines in the induction and resolution of experimental autoimmune encephalomyelitis
Cytokines in the induction and resolution of experimental autoimmune encephalomyelitis
复制标题
DOI：
10.1016/j.cyto.2005.07.012
复制
发表时间：
2005-10-21
期刊：
影响因子：
3.8
通讯作者：
Anderton, SM
中科院分区：
文献类型：
--
作者：
McGeachy, MJ;Anderton, SM
实验性自身免疫性脑脊髓炎是典型的T细胞介导的自身免疫性疾病模型。传统上，这种疾病被认为是1型与2型免疫：1型细胞因子IFN γ和TNF α促进疾病，而IL-4主导的2型反应是保护性的。然而，基因敲除小鼠的研究并不支持这种模式。最近的数据指出IL-23和IL-17（而不是IL-12和IFN γ）在炎症性病变的建立和持续中的重要作用。IL-10似乎是介导恢复的主要细胞因子。IL-10的来源包括B细胞（最可能在外周淋巴器官中）。然而，中枢神经系统内产生IL-10的关键细胞是CD 4（+）CD 25（+）T细胞群，其具有调节功能并且对疾病的解决至关重要。(c)2005爱思唯尔有限公司保留所有权利。
Experimental autoimmune encephalomyelitis is the prototypic T cell-mediated autoimmune disease model. Classically, this disease was viewed in terms of type 1 versus type 2 immunity: the type 1 cytokines IFN gamma and TNF alpha promoting disease, whereas an IL-4-dominated, type 2 response was protective. However, studies in knockout mice do not support this paradigm. More recent data point to important roles for IL-23 and IL-17 (rather than IL-12 and IFN gamma) in the establishment and persistence of the inflammatory lesion. IL-10 appears to be the dominant cytokine mediating recovery. The source of IL-10 includes B cells (most probably in the peripheral lymphoid organs). However, the key IL-10-producing cell within the central nervous system is a CD4(+)CD25(+) T cell population that has regulatory function and is critical to resolution of the disease. (c) 2005 Elsevier Ltd. All rights reserved.