[PDF][PDF] Intestinal bacterial colonization induces mutualistic regulatory T cell responses

MB Geuking, J Cahenzli, MAE Lawson, DCK Ng… - Immunity, 2011 - cell.com
MB Geuking, J Cahenzli, MAE Lawson, DCK Ng, E Slack, S Hapfelmeier, KD McCoy…
Immunity, 2011cell.com
Mammals harbor a dense commensal microbiota in the colon. Regulatory T (Treg) cells are
known to limit microbe-triggered intestinal inflammation and the CD4+ T cell compartment is
shaped by the presence of particular microbes or bacterial compounds. It is, however,
difficult to distinguish whether these effects reflect true mutualistic immune adaptation to
intestinal colonization or rather idiosyncratic immune responses. To investigate truly
mutualistic CD4+ T cell adaptation, we used the altered Schaedler flora (ASF). Intestinal …
Summary
Mammals harbor a dense commensal microbiota in the colon. Regulatory T (Treg) cells are known to limit microbe-triggered intestinal inflammation and the CD4+ T cell compartment is shaped by the presence of particular microbes or bacterial compounds. It is, however, difficult to distinguish whether these effects reflect true mutualistic immune adaptation to intestinal colonization or rather idiosyncratic immune responses. To investigate truly mutualistic CD4+ T cell adaptation, we used the altered Schaedler flora (ASF). Intestinal colonization resulted in activation and de novo generation of colonic Treg cells. Failure to activate Treg cells resulted in the induction of T helper 17 (Th17) and Th1 cell responses, which was reversed by wild-type Treg cells. Efficient Treg cell induction was also required to maintain intestinal homeostasis upon dextran sulfate sodium-mediated damage in the colon. Thus, microbiota colonization-induced Treg cell responses are a fundamental intrinsic mechanism to induce and maintain host-intestinal microbial T cell mutualism.
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