异位生成的调节性T细胞控制粘膜TH2炎症
Steven Z Josefowicz1, Rachel E Niec, Hye Young Kim
1Howard Hughes Medical Institute and Immunology Program, Sloan Kettering Institute, New York, New York 10021, USA.
诱导调节性T (Treg) 细胞,而不是来自甲状腺的细胞,对于预防粘膜部位的过敏炎症和维持肠道微生物群平衡至关重要. 它们的缺乏会导致像喘这样的过敏症.
科学领域:
- 免疫学 免疫学 免疫学
- 微生物学 微生物学
背景情况:
- 粘膜接口需要平衡促炎和抗炎反应,以防御病原体而不会引起过敏或炎症.
- 调节性T (Treg) 细胞,起源于胸腺 (tTreg) 或外围 (iTreg),对于免疫常态稳定和预防自身免疫至关重要.
研究的目的:
- 为了研究由胸腺衍生 (tTreg) 和诱导 (iTreg) 调节性T细胞在维持粘膜表面的免疫平衡中的不同作用.
- 确定iTreg细胞是否对于预防过敏炎症和维持肠道微生物群组成至关重要.
主要方法:
- 在小鼠中选择性阻断诱导调节性T (iTreg) 细胞分化.
- 评估自身免疫病理,T辅助细胞反应 (T,H1,T,H17,T,H2) 和粘膜炎症.
- 对iTreg缺乏小鼠肠道微生物群落组成的分析.
主要成果:
- 缺乏iTreg细胞的小鼠没有发展系统性自身免疫或恶化的T (H) 1 / T (H) 17反应.
- iTreg细胞缺乏导致胃肠道和肺部显著的T(H) 2型过敏炎症.
- 缺少iTreg细胞改变了肠道微生物群的组成.
结论:
- 来自胸腺的Treg细胞足以控制系统性自身免疫.
- 外型iTreg细胞在抑制粘膜过敏炎症和调节肠道微生物群方面发挥着关键的,独特的作用.
- 了解iTreg细胞功能是解决过敏性疾病和肠道失调症的关键.
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