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Experimental colitis in IL-10-deficient mice ameliorates in the absence of PTPN22.

08:00 EDT 13th June 2019 | BioPortfolio

Summary of "Experimental colitis in IL-10-deficient mice ameliorates in the absence of PTPN22."

Interleukin (IL)-10 plays key role in controlling intestinal inflammation. IL-10-deficient mice and patients with mutations in IL-10 or its receptor, IL-10R, show increased susceptibility to inflammatory bowel diseases (IBD). Protein tyrosine phosphatase PTPN22 controls immune cell activation and the equilibrium between regulatory and effector T cells, playing important role in controlling immune homeostasis of the gut. Here, we examined the role of PTPN22 in intestinal inflammation of IL-10-deficient (IL-10 ) mice. We crossed IL-10 mice with PTPN22 mice to generate PTPN22 IL-10 double knock-out mice and induced colitis with dextran-sodium sulfate (DSS). In line with previous reports, DSS-induced acute and chronic colitis was exacerbated in IL-10 mice as compared to wild-type (WT) controls. However, PTPN22 IL-10 double knock-out mice developed milder disease as compared to IL-10 mice. IL-17-promoting innate cytokines and Th17 cells were markedly increased in PTPN22 IL-10 mice, but did not provide a protective function. CXCL1/KC was also increased in PTPN22 IL-10 mice, but therapeutic injection of CXCL1/KC in IL-10 mice did not ameliorate colitis. These results show that PTPN22 promotes intestinal inflammation in IL-10-deficient mice, suggesting that therapeutic targeting of PTPN22 might be beneficial in patients with IBD and mutations in IL-10 and IL-10R. This article is protected by copyright. All rights reserved.

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Name: Clinical and experimental immunology
ISSN: 1365-2249
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