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Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes
Published on: September 26, 2013
介素-22,一个T(H) 17细胞因子,调解IL-23-诱导的皮肤炎症和阿坎托斯症
Yan Zheng1, Dimitry M Danilenko, Patricia Valdez
1Department of Immunology, Genentech, Inc., South San Francisco, California 94080, USA.
Nature
|December 26, 2006
概括
交白素-22 (IL-22),由T助手17 (T(H) 17) 细胞产生,在牛皮中驱动表皮层增生 (). 这种细胞因子通过Stat3激活来调解IL-23诱导的皮肤炎症和阿坎托斯.
科学领域:
- 免疫学 免疫学 免疫学
- 皮肤病学 皮肤病学
- 分子生物学分子生物学
背景情况:
- 牛皮是一种慢性炎症性皮肤疾病,其表现为表皮层增生 (acanthosis).
- 正确的驱动牛皮发病的机制尚不清楚.
- 干白素-23 (IL-23) 和T辅助细胞17 (T(H) 17) 参与了牛皮的发病.
研究的目的:
- 为了研究IL-22在IL-23介导的牛皮皮肤变化的作用.
- 阐明T(H) 17细胞对IL-22和IL-17产生的调节.
- 为了确定参与IL-22功能的下游信号通路.
主要方法:
- 从用IL-23或IL-6刺激的小鼠和人类原始T细胞中分析IL-22和IL-17的产生.
- 研究转化生长因子-β (TGF-β) 对IL-22和IL-17产生的影响.
- 通过Stat3激活评估IL-22在IL-23诱导的炎和皮肤炎症中的IL-22作用的体内研究.
主要成果:
- IL-22主要由T(H) 17细胞产生,并由IL-23或IL-6直接诱导.
- TGF-β抑制了IL-22的产生,同时促进了IL-17的产生,表明了差异调节.
- IL-22通过活体激活Stat3来调解IL-23诱导的和皮肤炎症.
结论:
- 通过IL-22和IL-17,T(H) 17细胞在宿主防御和牛皮等自身免疫性疾病中起着重要的作用.
- 在皮肤炎症中,IL-22作为一个关键的效应细胞因子,调解免疫系统-上皮细胞交叉交互.
- 准IL-22可能为牛皮和相关的炎症性皮肤疾病提供治疗策略.
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