| Literature DB >> 26329427 |
J C Martin1,2,3, G Bériou1, M Heslan1, C Bossard2,4,5, A Jarry4, A Abidi1, P Hulin6, S Ménoret1, R Thinard1, I Anegon1, C Jacqueline7, B Lardeux8, F Halary1, J-C Renauld9,10, A Bourreille8,11, R Josien1,2,3.
Abstract
Crohn's disease and ulcerative colitis, the two major forms of inflammatory bowel diseases (IBDs), are characterized by high levels of IL-22 production. Rodent studies revealed that this cytokine is protective during colitis but whether this is true in IBDs is unclear. We show here that levels of the soluble inhibitor of IL-22, interleukin 22-binding protein (IL-22BP), are significantly enhanced during IBDs owing to increased numbers of IL-22BP-producing eosinophils, that we unexpectedly identify as the most abundant source of IL-22BP protein in human gut. In addition, using IL-22BP-deficient rats, we confirm that endogenous IL-22BP is effective at blocking protective actions of IL-22 during acute colitis. In conclusion, our study provides new important insights regarding the biology of IL-22 and IL-22BP in the gut and indicates that protective actions of IL-22 are likely to be suboptimal in IBDs thus making IL-22BP a new relevant therapeutic target.Entities:
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Year: 2015 PMID： 26329427 DOI： 10.1038/mi.2015.83
Source DB: PubMed Journal: Mucosal Immunol ISSN： 1933-0219 Impact factor: 7.313