論文

国際誌
2007年12月

Blocking of IL-6 signaling pathway prevents CD4+ T cell-mediated colitis in a T(h)17-independent manner.

International immunology
  • Daisuke Noguchi
  • ,
  • Daiko Wakita
  • ,
  • Masaki Tajima
  • ,
  • Shigeru Ashino
  • ,
  • Yoichiro Iwakura
  • ,
  • Yue Zhang
  • ,
  • Kenji Chamoto
  • ,
  • Hidemitsu Kitamura
  • ,
  • Takashi Nishimura

19
12
開始ページ
1431
終了ページ
40
記述言語
英語
掲載種別
研究論文(学術雑誌)

Naive CD4(+) T cells rapidly proliferate to generate effector cells after encountering an antigen and small numbers survive as memory T cells in preparation for future immunological events. In the present work, adoptive transfer of naive CD4(+) T cells into RAG2(-/-) mice caused the generation of memory-type effector T cells including T(h)1, T(h)2, T(h)17 and regulatory T cells, and eventually induced T cell-dependent colitis. We found here that blocking of the IL-6R with a specific mAb remarkably inhibited the CD4(+) T cell-mediated colitis in parallel with the inhibition of T(h)17 cell generation. However, the transfer of naive CD4(+) T cells prepared from IL-17(-/-) mice still induced severe colitis. At the effector phase, the mAb significantly inhibited IL-17 but not IFN-gamma production. The blockade of IL-6 signaling enhanced the generation of IL-4- and IL-10-producing CD4(+) T cells, and inhibited up-regulation of tumor necrosis factor -alpha mRNA expression in the colon. These findings clearly demonstrated that IL-6 is a critical factor for the induction of colitis by expansion of naive CD4(+) T cells in RAG2(-/-) mice. Thus, the IL-6-mediated signaling pathway may be a significant therapeutic target in T cell-mediated autoimmune diseases.

リンク情報
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/17981790
ID情報
  • ISSN : 0953-8178
  • PubMed ID : 17981790

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