Homeostatic IL-23 receptor signaling limits Th17 response through IL-22-mediated containment of commensal microbiota.

ABSTRACT: Mammalian hosts are colonized with commensal microbes in various mucosal and epithelial tissues, including the intestinal tract. In mice, the presence of segmented filamentous bacteria (SFB) promotes Th17 differentiation and the development of autoimmune disease. Here, we demonstrate that the IL-23 pathway dynamically regulates the abundance of SFB as well as mucosal barrier function in the adult animal. Genetic or pharmacological inactivation of the pathway selectively perturbs the abundance of a small group of commensals, including SFB, and results in an impaired mucosal barrier. Defective barrier function leads to systemic dissemination of microbial products, provoking induction of the IL-23 pathway with dual consequences: IL-23 drives IL-22 production to reinforce mucosal barrier funct

SUBMITTER: Shih VF 

PROVIDER: S-EPMC4183330 | biostudies-literature | 2014 Sep

REPOSITORIES: biostudies-literature