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      Intestinal interleukin-17 receptor signaling mediates reciprocal control of the gut microbiota and autoimmune inflammation

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          Summary

          Interleukin-17 (IL-17) and IL-17 receptor (IL-17R) signaling are essential for regulating mucosal host defense against many invading pathogens. Commensal bacteria, especially segmented filamentous bacteria (SFB), are a crucial factor that drives T helper 17 (Th17) cell development in the gastrointestinal tract. In this study, we demonstrate that Th17 cells controlled SFB burden. Disruption of IL-17R signaling in the enteric epithelium resulted in SFB dysbiosis due to reduced expression of α-defensins, Pigr and Nox1. When subjected to experimental autoimmune encephalomyelitis, IL-17R signaling deficient mice demonstrated earlier disease onset and worsened severity that was associated with increased intestinal Csf2 expression and elevated systemic GM-CSF cytokine concentrations. Conditional deletion of IL-17R in the enteric epithelium demonstrated that there was a reciprocal relationship between the gut microbiota and enteric IL-17R signaling that controlled dysbiosis, constrained Th17 development, and regulated the susceptibility to autoimmune inflammation.

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          Author and article information

          Journal
          9432918
          8591
          Immunity
          Immunity
          Immunity
          1074-7613
          1097-4180
          17 February 2016
          15 March 2016
          15 March 2017
          : 44
          : 3
          : 659-671
          Affiliations
          [1 ]Richard King Mellon Foundation Institute for Pediatric Research, Children’s Hospital of Pittsburgh of UPMC, University of Pittsburgh, Pittsburgh, PA 15224, USA
          [2 ]Department of Civil and Environmental Engineering, University of Pittsburgh, Pittsburgh, PA 15261, USA
          [3 ]Center for Vaccine Research, University of Pittsburgh, Pittsburgh, PA 15261, USA
          [4 ]Division of Pediatric Gastroenterology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA
          [5 ]Center for Immunology & Microbial Disease Albany Medical College, Albany, NY 12208, USA
          Author notes
          Correspondence: Jay.Kolls@ 123456chp.edu , Jay K. Kolls, MD, Director, Richard King Mellon Foundation Institute for Pediatric Research, Professor of Pediatrics, University of Pittsburgh School of Medicine, Vice Chair for Translational Research, Department of Pediatrics, Children’s Hospital of Pittsburgh of UPMC, Ph. 412-692-7710, Fax. 412-692-7636
          Article
          PMC4794750 PMC4794750 4794750 nihpa759876
          10.1016/j.immuni.2016.02.007
          4794750
          26982366
          55266ecc-d426-4b3a-a0cc-0a2ed1748d0d
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