11月13日的Science文章报道：在对环境因素启动的应答中，不同种类保护性免疫是被STAT 转录因子家族成员的激活所致。CD4+ 调节性T细胞 (Tregs) 抑制过度的免疫应答，并且它们的缺陷导致一致死性的、通过TH1和TH2 CD4+T细胞介导损伤而导致的多器官自身免疫综合症。作者研究显示在小鼠病理性TH17应答中，同样受Tregs 的限制。这种抑制将随着Tregs 中一种TH17分化转录因子Stat3的消失而解除，并且导致致死性肠道炎症。
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Science 13 November 2009:
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Reports
CD4+ Regulatory T Cells Control TH17 Responses in a Stat3-Dependent Manner
Ashutosh Chaudhry,1,2 Dipayan Rudra,1,2 Piper Treuting,3 Robert M. Samstein,1 Yuqiong Liang,1 Arnold Kas,2 Alexander Y. Rudensky1,2,*
Distinct classes of protective immunity are guided by activation of STAT transcription factor family members in response to environmental cues. CD4+ regulatory T cells (Tregs) suppress excessive immune responses, and their deficiency results in a lethal, multi-organ autoimmune syndrome characterized by T helper 1 (TH1) and T helper 2 (TH2) CD4+ T cell–dominated lesions. Here we show that pathogenic TH17 responses in mice are also restrained by Tregs. This suppression was lost upon Treg-specific ablation of Stat3, a transcription factor critical for TH17 differentiation, and resulted in the development of a fatal intestinal inflammation. These findings suggest that Tregs adapt to their environment by engaging distinct effector response–specific suppression modalities upon activation of STAT proteins that direct the corresponding class of the immune response.
http://www.sciencemag.org/cgi/content/abstract/326/5955/986
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