Cutting edge: mTORC1 in intestinal CD11c +CD11b + dendritic cells regulates intestinal homeostasis by promoting IL-10 production

Masashi Ohtani, Takayuki Hoshii, Hideki Fujii, Shigeo Koyasu, Atsushi Hirao, Satoshi Matsuda

研究成果: Article査読

67 被引用数 (Scopus)

抄録

The mammalian target of rapamycin (mTOR) controls cell growth and survival through two distinct complexes called mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2). Although several reports have suggested the involvement ofmTORC1in development and function of dendritic cells (DCs), its physiological roles remain obscure. We therefore established mTORC1 signal-deficient mice lacking Raptor, an essential component of mTORC1 signal, specifically in DC lineage (referred to here as Raptor DC-/-). Raptor DC-/- mice exhibited cell expansion in specific subsets of DCs such as splenic CD8 + DCs and intestinal CD11c +CD11b +DCs. We also found that impaired mTORC1 signal resulted in the suppression of IL-10 production along with enhanced CD86 expression in intestinal CD11c +CD11b + DCs and that Raptor DC-/- mice were highly susceptible to dextran sodium sulfate-induced colitis. Our results uncover mTORC1-mediated anti-inflammatory programs in intestinal CD11c +CD11b +DCs to limit the intestinal inflammation.

本文言語English
ページ(範囲)4736-4740
ページ数5
ジャーナルJournal of Immunology
188
10
DOI
出版ステータスPublished - 2012 5月 15

ASJC Scopus subject areas

  • 免疫アレルギー学
  • 免疫学

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