Getting to the crux of the matter: IL-23 and Th17 cell accumulation in the CNS.

Getting to the crux of the matter: IL-23 and Th17 cell accumulation in the CNS.
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DOI:
10.1002/eji.200939675
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发表时间:
2009-07
影响因子:
5.4
通讯作者:
Segal, Benjamin M.
Segal, Benjamin M.
中科院分区:
医学3区
文献类型:
--
作者:
Segal, Benjamin M.
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IL-23在用髓鞘少突胶质细胞糖蛋白(MOG 35 -55)的免疫显性表位主动免疫C57 BL/6小鼠诱导的实验性自身免疫性脑脊髓炎(EAE)中起关键作用。最初认为IL-23的致病作用与自身反应性CD 4 + Th 17细胞的产生、扩增和/或稳定直接相关。然而,最近的一些研究已经发现,在EAE的发展中,与Th 17细胞或其产物(IL-17 A、IL-17 F和IL-22)相反,IL-23的需求之间存在差异。在本期《欧洲免疫学杂志》中,Gabor及其同事证明,IL-23信号传导的受损不会阻碍外周淋巴组织中髓鞘特异性CD 4 + T细胞的扩增,但会抑制它们在CNS中的积累。这篇论文有助于越来越多的数据,暗示IL-23在收购中枢神经系统归巢的自身反应性效应细胞的属性。
IL-23 plays a critical role in experimental autoimmune encephalomyelitis (EAE) induced by the active immunization of C57BL/6 mice with an immunodominant epitope of myelin oligodendrocyte glycoprotein (MOG35-55). It was initially assumed that the pathogenic effects of IL-23 were directly related to the generation, expansion and/ or stabilization of autoreactive CD4+ Th17 cells. However, a number of recent studies have uncovered discepancies between the requirement for IL-23, as opposed to Th17 cells or their products (IL-17A, IL-17F and IL-22), in the development of EAE. In this issue of the European Journal of Immunology, Gabor and colleagues demonstrate that impairment of IL-23 signaling does not impede the expansion of myelin-specific CD4+ T cells in peripheral lymphoid tissues but inhibits their accumulation in the CNS. This paper contributes to a growing body of data that implicates IL-23 in the acquisition of CNS homing properties by autoreactive effector cells.
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