RORγt-Raftlin1 complex regulates the pathogenicity of Th17 cells and intestinal inflammation.

نویسندگان

چکیده

Abstract Th17 cells that produce IL-17 are pathogenic in many human diseases, including inflammatory bowel disease (IBD), but are, paradoxically, essential for maintaining the integrity of intestinal barrier a non-inflammatory state. However, intracellular mechanisms regulate distinct transcriptional profiles and functional diversity remain unclear. We have found Raftlin1, lipid raft protein, is specifically upregulated forms complex with RORγt via its conserved LLNSL motif cells. Disruption RORγt-Raftlin1 Raftlin1 ΔLLNSLknock-in mice resulted attenuated elicited by Citrobacter rodentium; however, there was no effect on nonpathogenic induced commensal segmented filamentous bacteria (SFB). Mechanistically, we recruits phospholipids to promotes pathogenicity Thus, identified fundamental mechanism drives function cells, which could provide platform new therapeutic strategies dampen Th17-mediated diseases. This work supported funds from National Institutes Health (R01-DK115668, R01-AI155786) Cancer Prevention Research Institute Texas (RP190527) stimulus grant Harold C. Simmons Comprehensive Center, UT Southwestern Medical Center.

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ژورنال

عنوان ژورنال: Journal of Immunology

سال: 2023

ISSN: ['1550-6606', '0022-1767']

DOI: https://doi.org/10.4049/jimmunol.210.supp.154.03