Homeostatic IL-23 receptor signaling limits Th17 response through IL-22-mediated containment of commensal microbiota
Abstract
Commensal microbiota are known to be required for the elicitation of host Th17 responses, which may mediate autoimmune diseases. Here, we demonstrate that the IL-23 pathway dynamically regulates the abundance of certain commensals and maintains barrier function. Barrier disruption results in systemic dissemination of microbial products, which invokes the IL-23 pathway, with both beneficial and potentially deleterious consequences. Through induction of IL-22, IL-23 contributes to barrier repair, and through induction of the Th17 response, it aims to neutralize escaped commensal microbes. Thus, barrier disruption results in a pro-Th17 environment in which not only antimicrobial but also potentially antihost Th17 cells can develop.
- Publication:
-
Proceedings of the National Academy of Science
- Pub Date:
- September 2014
- DOI:
- 10.1073/pnas.1323852111
- Bibcode:
- 2014PNAS..11113942S