感染的细胞的天生的免疫识别指导T(H) 17细胞分化
Miriam Beer Torchinsky1, Johan Garaude, Andrea P Martin
1Immunology Institute, Department of Medicine, Mount Sinai School of Medicine, 1425 Madison Avenue, New York, New York 10029, USA.
Nature
|March 6, 2009
概括
天生的免疫细胞识别受感染的亡细胞,触发T助手17 (T(H) 17细胞的分化. 这一过程对于宿主防御至关重要,但也可能与自身免疫性疾病有关.
科学领域:
- 免疫学 免疫学 免疫学
- 细胞生物学 细胞生物学
- 微生物学 微生物学
背景情况:
- 适应性免疫涉及CD4 T辅助细胞分化为子集,如T辅助1 (T(H) 1),T辅助2 (T(H) 2和最近发现的T辅助17 (T(H) 17) 细胞.
- T(H) 17细胞对于宿主对病原体的防御至关重要.
- 实验室研究表明,转化生长因子-β (TGF-β) 和互白素-6 (IL-6) 诱导T(H) 17分化,而IL-23促进它们的扩张,但实验室触发因素尚不清楚.
研究的目的:
- 阐明诱导T(H) 17细胞分化所需的细胞因子组合的体内条件.
- 为了研究受感染的亡细胞在启动T(H) 17免疫反应中的作用.
- 探索T(H) 17细胞,自身免疫和病原体诱导的亡之间的联系.
主要方法:
- 研究了小鼠和人类系统中的树突细胞和受感染的亡细胞之间的相互作用.
- 在小鼠中利用Citrobacter rodentium感染模型研究肠道表皮中的T(H) 17反应.
- 分析了细胞因子的产生和T细胞的分化,在有或没有微生物信号的apoptotic细胞的 fagocytosis之后.
主要成果:
- 被树突细胞感染的瘤细胞的细胞分裂独特地触发了协同作用的TGF-β和IL-6的产生.
- 识别病原体相关的分子模式和酸在细胞中介介于这种细胞因子的诱导.
- 在感染期间阻断亡会损害T(H) 17分化,而非受感染的亡细胞的化会促进调控性T细胞分化.
结论:
- 受感染的亡细胞是关键的先天性免疫信号,指导T(H) 17细胞分化.
- 诱导亡的病原体可能会优先引起T(H) 17介导的免疫.
- 了解感染的亡细胞的识别方式,可以揭示自身免疫性疾病的机制.
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