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10.1016/j.immuni.2016.02.019

http://scihub22266oqcxt.onion/10.1016/j.immuni.2016.02.019
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suck abstract from ncbi


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pmid26982365      Immunity 2016 ; 44 (3): 634-46
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  • Lymphoid tissue-resident commensal bacteria promote members of the IL-10 cytokine family to establish mutualism #MMPMID26982365
  • Fung TC; Bessman NJ; Hepworth MR; Kumar N; Shibata N; Kobuley D; Wang K; Ziegler CGK; Goc J; Shima T; Umesaki Y; Sartor RB; Sullivan KV; Lawley TD; Kunisawa J; Kiyono H; Sonnenberg GF
  • Immunity 2016[Mar]; 44 (3): 634-46 PMID26982365show ga
  • Physical separation between the mammalian immune system and commensal bacteria is necessary to limit chronic inflammation. However, selective species of commensal bacteria can reside within intestinal-associated lymphoid tissues of healthy mammals. Here, we demonstrate that lymphoid tissue-resident commensal bacteria (LRC) colonized murine dendritic cells and modulate their cytokine production. In germ-free and antibiotic-treated mice, LRCs colonized intestinal-associated lymphoid tissues and induced multiple members of the IL-10 cytokine family, including dendritic cell-derived IL-10 and group 3 innate lymphoid cell (ILC3)-derived IL-22. Notably, IL-10 limited the development of pro-inflammatory Th17 cell responses, and IL-22 production enhanced LRC colonization in the steady state. Furthermore, LRC colonization protected mice from lethal intestinal damage in an IL-10-IL-10R-dependent manner. Collectively, our data reveal a unique host-commensal bacteria dialogue whereby selective subsets of commensal bacteria interact with dendritic cells to facilitate tissue-specific responses that are mutually beneficial for both the host and the microbe.
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