期刊
JOURNAL OF IMMUNOLOGY
卷 188, 期 10, 页码 4736-4740出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1200069
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资金
- Japan Society for the Promotion of Science [23790546, 22590437, 22590439]
- Kansai Medical University
- Takeda Science Foundation
- Grants-in-Aid for Scientific Research [23130507, 24790967, 23650593, 22590439, 23790546, 21390290, 22590437, 22790906] Funding Source: KAKEN
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 of mTORC1 in 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-/-)). Rapto(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. The Journal of Immunology, 2012, 188: 4736-4740.
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