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. 2018 Apr 25;9:885. doi: 10.3389/fimmu.2018.00885

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Copyright © 2018 Reinhardt and Prinz.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Involvement of interleukin (IL)-17/IL-22-producing lymphocytes in spondyloarthritis (SpA)-associated inflammation. Genetic and epigenetic predisposition, altered microbial composition, and entheseal microdamage can influence the induction and progression of tissue inflammation in SpA. In addition to tissue-resident γδ T cells and ILC3s, circulating and/or gut-derived γδ T cells, ILC3s, T_H17 cells, or mucosal-associated invariant T (MAIT) cells might promote IL-23-driven joint inflammation by producing increased amounts of IL-17 and IL-22.