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The oxysterol receptor GPR183 in inflammatory bowel diseases

期刊

BRITISH JOURNAL OF PHARMACOLOGY
卷 178, 期 16, 页码 3140-3156

出版社

WILEY
DOI: 10.1111/bph.15311

关键词

colitis; EBI2; GPR183; inflammatory bowel diseases; innate lymphoid cells; oxysterols; solitary intestinal lymphoid tissue; Ubac2

资金

  1. German Research Foundation (DFG) [403224013 - SFB 1382 (B06) 403224013]
  2. Swiss National Science Foundation [32473B_156525, 310030_192738, 323630-183987]
  3. Swiss National Science Foundation (SNF) [32473B_156525, 310030_192738] Funding Source: Swiss National Science Foundation (SNF)

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The oxysterol receptor GPR183 and its ligands play a crucial role in immune cell positioning and migration in inflammatory bowel disease. Targeting GPR183-dependent cell migration could be a potential therapeutic strategy for IBD.
Immune cell trafficking is an important mechanism for the pathogenesis of inflammatory bowel disease (IBD). The oxysterol receptor GPR183 and its ligands, dihydroxylated oxysterols, can mediate positioning of immune cells including innate lymphoid cells. GPR183 has been mapped to an IBD risk locus, however another gene, Ubac2 is encoded on the reverse strand and associated with Behcet's disease, therefore the role of GPR183 as a genetic risk factor requires validation. GPR183 and production of its oxysterol ligands are up-regulated in human IBD and murine colitis. Gpr183 inactivation reduced severity of colitis in group 3 innate lymphoid cells-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.

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