控制T ((reg) 和T ((H)) 17细胞分化通过烯碳化合物受体的控制
Francisco J Quintana1, Alexandre S Basso, Antonio H Iglesias
1Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, Massachusetts 02115, USA.
Nature
|March 26, 2008
概括
基碳化合物受体 (AHR) 调节调节性T (Treg) 细胞和促炎性T (TH17) 细胞之间的平衡. 它的连接体特异性作用为自身免疫性疾病治疗提供了一个新的点.
科学领域:
- 免疫学 免疫学 免疫学
- 分子生物学分子生物学
- 自免疫性疾病 自免疫性疾病
背景情况:
- 调节性T (Treg) 细胞和T辅助细胞17 (TH17) 具有相互的发育途径.
- 对Treg和TH17细胞的失调与自身免疫性疾病有关.
- 在Treg和TH17细胞生成的生理调节者仍然在很大程度上是未知的.
研究的目的:
- 为了确定Treg和TH17细胞分化的关键调节者.
- 为了研究基碳化合物受体 (AHR) 在免疫细胞系中的作用.
- 探索AHR作为免疫调节的潜在治疗点.
主要方法:
- 在小鼠模型中研究了酸受体 (AHR) 的作用.
- 利用特定的AHR配体调节T细胞分化.
- 评估了AHR激活对实验性自身免疫脑膜炎 (EAE) 严重性的影响.
主要成果:
- 由2,3,7,8-四二二子二氧化激活AHR促进了功能Treg细胞,并抑制了EAE.
- 通过6-formylindolo[3,2-b]carbazole激活AHR抑制了Treg发育并增强了TH17分化,恶化了EAE.
- AHR证明了对Treg和TH17细胞分化的依赖体调节.
结论:
- 基碳化合物受体 (AHR) 是Treg和TH17细胞平衡的关键调节器.
- 在自身免疫性疾病中,AHR的联体特异性活性为治疗性免疫调节提供了一个独特的机制.
- 针对AHR提供了一个有前途的战略,用于开发针对自身免疫疾病的新型治疗方法.
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