Publication date: Available online 3 July 2018
Source:Immunity
Author(s): Myunghoo Kim, Carolina Galan, Andrea A. Hill, Wan-Jung Wu, Hannah Fehlner-Peach, Hyo Won Song, Deborah Schady, Matthew L. Bettini, Kenneth W. Simpson, Randy S. Longman, Dan R. Littman, Gretchen E. Diehl
The intestinal barrier is vulnerable to damage by microbiota-induced inflammation that is normally restrained through mechanisms promoting homeostasis. Such disruptions contribute to autoimmune and inflammatory diseases including inflammatory bowel disease. We identified a regulatory loop whereby, in the presence of the normal microbiota, intestinal antigen-presenting cells (APCs) expressing the chemokine receptor CX3CR1 reduced expansion of intestinal microbe-specific T helper 1 (Th1) cells and promoted generation of regulatory T cells responsive to food antigens and the microbiota itself. We identified that disruption of the microbiota resulted in CX3CR1+ APC-dependent inflammatory Th1 cell responses with increased pathology after pathogen infection. Colonization with microbes that can adhere to the epithelium was able to compensate for intestinal microbiota loss, indicating that although microbial interactions with the epithelium can be pathogenic, they can also activate homeostatic regulatory mechanisms. Our results identify a cellular mechanism by which the microbiota limits intestinal inflammation and promotes tissue homeostasis.
Graphical abstract
Teaser
Host microbiota interactions regulate many aspects of immunity. Kim et al. demonstrate that microbial adhesion to intestinal epithelium helps regulate the balance between pro- and anti-inflammatory T cell responses through induction of IL-10 by a subset of intestinal antigen-presenting cells.https://ift.tt/2INSwut
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