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Intestinal Interleukin-17 Receptor Signaling Mediates Reciprocal Control of the Gut Microbiota and Autoimmune Inflammation.

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2016

Immunity. 2016 Mar 15;44(3):659-71. doi: 10.1016/j.immuni.2016.02.007.

Intestinal Interleukin-17 Receptor Signaling Mediates Reciprocal Control of the Gut Microbiota and Autoimmune Inflammation.

P Kumar;L Monin;P Castillo;W Elsegeiny;W Horne;T Eddens;A Vikram;M Good;AA Schoenborn;K Bibby;RC Montelaro;DW Metzger;AS Gulati;JK Kolls

University of Pittsburgh, Pittsburgh, PA 15224, USA. University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA. Albany Medical College, Albany, NY 12208, USA.

Service type: Knockout mice

Abstract

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 cell development, and regulated the susceptibility to autoimmune inflammation.

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