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在实验性自身免疫性脑脊髓炎中，产生干扰素-γ的Th1亚群是白细胞介素-17的主要来源。

An interferon-gamma-producing Th1 subset is the major source of IL-17 in experimental autoimmune encephalitis.

作者信息

Suryani Santi, Sutton Ian

机构信息

The Garvan Institute of Medical Research, Department of Inflammation, 384 Victoria Street, Darlinghurst, Sydney, NSW 2010, Australia.

出版信息

J Neuroimmunol. 2007 Feb;183(1-2):96-103. doi: 10.1016/j.jneuroim.2006.11.023. Epub 2007 Jan 22.

DOI:10.1016/j.jneuroim.2006.11.023
PMID:17240458
Abstract

ThIL-17 (IL-17+/IFN-gamma-) cell lines are significantly more encephalitogenic than Th1 (IL-17-/IFN-gamma+) cell lines in adoptive transfer EAE models. In actively induced EAE short ex vivo peptide stimulation identifies an IL-17+/IFN-gamma+ population of CD4+ CNS-infiltrating MOG35-55-specific T cells, which outnumber IL-17+/IFN-gamma- cells by approximately 3:1 as disease develops. A decrease in numbers of IL-17+/IFN-gamma+ cells following in vitro culture is accompanied by an increase in IL-17-/IFN-gamma+ cell numbers. Together these ex vivo and in vitro observations imply that the Th1 lineage is more encephalitogenic than is suggested by adoptive transfer of Th1 (IL-17-/IFN-gamma+) cell lines which have been terminally differentiated in vitro.

摘要

在过继转移实验性自身免疫性脑脊髓炎（EAE）模型中，Th17（IL-17+/IFN-γ-）细胞系比Th1（IL-17-/IFN-γ+）细胞系具有更强的致脑炎性。在主动诱导的EAE中，短时间的体外肽刺激可鉴定出一群IL-17+/IFN-γ+的CD4+中枢神经系统浸润性MOG35-55特异性T细胞，随着疾病发展，其数量比IL-17+/IFN-γ-细胞多出约3倍。体外培养后IL-17+/IFN-γ+细胞数量减少的同时，IL-17-/IFN-γ+细胞数量增加。这些体内外观察结果共同表明，Th1谱系的致脑炎性比体外终末分化的Th1（IL-17-/IFN-γ+）细胞系过继转移所显示的更强。

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