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- W4313305905 abstract "Abstract IL-22 acts on epithelia, hepatocytes and pancreatic cells and stimulates innate immunity, tissue protection and repair. IL-22 may also cause inflammation and abnormal cell proliferation. The binding of IL-22 to its receptor is competed by IL-22BP. We addressed the question of the role of IL-22 and IL-22BP in hepatic fibrosis caused by schistosomes or by HCV. We found that schistosome eggs stimulate the production of IL-22 transcripts and inhibit the accumulation of IL22-BP transcripts in schistosome-infected mice and that schistosome eggs selectively stimulate the production of IL-22 by blood leukocytes from individuals chronically infected with S.japonicum. High IL-22 levels in cultures correlated with protection against hepatic fibrosis and portal hypertension. To test further the implication of IL-22/IL-22BP in hepatic disease, we analyzed common genetic variants of IL22RA2, which encodes IL-22BP, and found that the genotypes AA, GG of rs6570136 (p=0.003; OR=2), and CC, TT of rs2064501 (p=0.01; OR=2), were associated with severe fibrosis in Chinese infected with S.japonicum. We confirmed this result in Sudanese and Brazilians infected with S.mansoni. The aggravating genotypes were associated with high IL22RA2 transcripts levels. These same variants were also associated with HCV-induced fibrosis and cirrhosis. These results provide strong evidence that IL-22 protects against and IL-22BP aggravates liver fibrosis and cirrhosis in humans with chronic liver infections." @default.
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- W4313305905 date "2015-05-01" @default.
- W4313305905 modified "2023-10-06" @default.
- W4313305905 title "IL-22 and IL-22 binding protein (IL-22BP) regulate fibrosis and cirrhosis in hepatitis C virus and schistosome infections (CCR4P.202)" @default.
- W4313305905 doi "https://doi.org/10.4049/jimmunol.194.supp.118.2" @default.
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