| Literature DB >> 25381358 |
Joseph H Chewning1, Casey T Weaver2.
Abstract
Th17 cells have emerged as important mediators of host defense and homeostasis at barrier sites, particularly the intestines, where the greatest number and diversity of the microbiota reside. A critical balance exists between protection of the host from its own microbiota and pathogens and the development of immune-mediated disease. Breaches of local innate immune defenses provide critical stimuli for the induction of Th17 cell development, and additional cues within these tissues promote Th17 cell survival and/or plasticity. Normally, this results in eradication of the microbial threat and restitution of homeostasis. When dysregulated, however, Th17 cells can cause a range of immune-mediated diseases, whether directed against Ags derived from the microbiota, such as in inflammatory bowel disease, or against self-Ags in a range of autoimmune diseases. This review highlights recent discoveries that provide new insights into ways in which environmental signals impact Th17 cell development and function in the intestines.Entities:
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Year: 2014 PMID: 25381358 PMCID: PMC6007010 DOI: 10.4049/jimmunol.1401835
Source DB: PubMed Journal: J Immunol ISSN: 0022-1767 Impact factor: 5.422