AI Article Synopsis
- The mammalian target of rapamycin (mTOR) regulates cell growth and survival through two complexes, mTORC1 and mTORC2, with mTORC1 playing a significant role in dendritic cell development and function.
- Researchers created mTORC1 signal-deficient mice (Raptor(DC-/-)) to study the specific effects of this signal in dendritic cells, revealing increased cell expansion in certain dendritic cell subsets.
- Findings indicated that mTORC1 signaling is crucial for limiting intestinal inflammation, as Raptor(DC-/-) mice showed suppressed IL-10 production and heightened vulnerability to colitis.
Article Abstract
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-/-)). 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.
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| http://dx.doi.org/10.4049/jimmunol.1200069 | DOI Listing |
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