CD4+ regulatory T cells control TH17 responses in a stat3-dependent manner Academic Article uri icon


MeSH Major

  • Inflammatory Bowel Diseases
  • STAT3 Transcription Factor
  • T-Lymphocyte Subsets
  • T-Lymphocytes, Helper-Inducer
  • T-Lymphocytes, Regulatory


  • Distinct classes of protective immunity are guided by activation of STAT transcription factor family members in response to environmental cues. CD4+ regulatory T cells (T(regs)) 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 T(regs). This suppression was lost upon T(reg)-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 T(regs) 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.

publication date

  • November 13, 2009



  • Academic Article



  • eng

PubMed Central ID

  • PMC4408196

Digital Object Identifier (DOI)

  • 10.1126/science.1172702

PubMed ID

  • 19797626

Additional Document Info

start page

  • 986

end page

  • 91


  • 326


  • 5955