The adaptor TRAF5 limits the differentiation of inflammatory CD4 + T cells by antagonizing signaling via the receptor for IL-6

Hiroyuki Nagashima, Yuko Okuyama, Atsuko Asao, Takeshi Kawabe, Satoshi Yamaki, Hiroyasu Nakano, Michael Croft, Naoto Ishii, Takanori So

研究成果: Article査読

26 被引用数 (Scopus)

抄録

The physiological functions of members of the tumor-necrosis factor (TNF) receptor (TNFR)-associated factor (TRAF) family in T cell immunity are not well understood. We found that in the presence of interleukin 6 (IL-6), naive TRAF5-deficient CD4 + T cells showed an enhanced ability to differentiate into the T H 17 subset of helper T cells. Accordingly, T H 17 cell-associated experimental autoimmune encephalomyelitis (EAE) was greatly exaggerated in Traf5 -/- mice. Although it is normally linked with TNFR signaling pathways, TRAF5 constitutively associated with a cytoplasmic region in the signal-transducing receptor gp130 that overlaps with the binding site for the transcription activator STAT3 and suppressed the recruitment and activation of STAT3 in response to IL-6. Our results identify TRAF5 as a negative regulator of the IL-6 receptor signaling pathway that limits the induction of proinflammatory CD4 + T cells that require IL-6 for their development.

本文言語English
ページ(範囲)449-456
ページ数8
ジャーナルNature Immunology
15
5
DOI
出版ステータスPublished - 2014 5

ASJC Scopus subject areas

  • 免疫アレルギー学
  • 免疫学

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