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.
中科院分区:
文献类型:
--
作者:
Segal, Benjamin M.
关键词:
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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