The oxysterol receptor GPR183 in inflammatory bowel diseases.

Details

Serval ID
serval:BIB_EFBB171F53C5
Type
Article: article from journal or magazin.
Publication sub-type
Review (review): journal as complete as possible of one specific subject, written based on exhaustive analyses from published work.
Collection
Publications
Institution
Title
The oxysterol receptor GPR183 in inflammatory bowel diseases.
Journal
British journal of pharmacology
Author(s)
Misselwitz B., Wyss A., Raselli T., Cerovic V., Sailer A.W., Krupka N., Ruiz F., Pot C., Pabst O.
ISSN
1476-5381 (Electronic)
ISSN-L
0007-1188
Publication state
In Press
Peer-reviewed
Oui
Language
english
Notes
Publication types: Journal Article ; Review
Publication Status: aheadofprint
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.
Keywords
EBI2, GPR183, UBAC2, colitis, inflammatory bowel diseases, innate lymphoid cells, oxysterols, solitary intestinal lymphoid tissue
Pubmed
Create date
09/11/2020 9:27
Last modification date
19/01/2021 7:26
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