The oxysterol receptor GPR183 in inflammatory bowel diseases.

DOI
Publisher DOI
PubMed ID
33145756
Abstract
Immune cell trafficking is an important mechanism for the pathogenesis of inflammatory bowel disease (IBD). The G-protein-coupled receptor 183 (GPR183, also called EBI2) and its ligands, dihydroxylated oxysterols can mediate positioning of immune cells including innate lymphoid cells (ILCs). GPR183 has been mapped to an IBD risk locus; however, another gene, UBAC2, is encoded on the reverse strand and associated with Behçet's disease and the role of GPR183 as a genetic risk factor requires validation. GPR183 and production of its oxysterol ligands are upregulated in human IBD and murine colitis. Gpr183 inactivation reduced severity of colitis in ILC3-dependent colitis and in IL-10 colitis but not in dextran sodium sulphate colitis. Irrespectively, Gpr183 knockout strongly reduced accumulation of intestinal lymphoid tissue in health and all colitis models. In conclusion, genetic, translational and experimental studies implicate GPR183 in IBD pathogenesis and GPR183-dependent cell migration might be a therapeutic drug target for IBD.
Date Issued
2021-08
Publication Type
Article
Subject(s)
Subjects
EBI2 GPR183 UBAC2 colitis inflammatory bowel diseases innate lymphoid cells oxysterols solitary intestinal lymphoid tissue
Language(s)
en
Author(s)
Wyss, Annika
Raselli, Tina
Cerovic, Vuc
Sailer, Andreas W
Ruiz, Florian
Pot, Caroline
Pabst, Oliver
Additional Credits
Journal
British journal of pharmacology
Publisher
Wiley-Blackwell
ISSN
0007-1188
Access(Rights)
open.access
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