A pathogenic role for T cell-derived IL-22BP in inflammatory bowel disease
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- Erscheinungsjahr:
- 2016
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- Beschreibung:
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Intestinal inflammation can impair mucosal healing, thereby establishing a vicious cycle leading to chronic inflammatory bowel disease (IBD). However, the signaling networks driving chronic inflammation remain unclear. Here we report that CD4(+) T cells isolated from patients with IBD produce high levels of interleukin-22 binding protein (IL-22BP), the endogenous inhibitor of the tissue-protective cytokine IL-22. Using mouse models, we demonstrate that IBD development requires T cell-derived IL-22BP. Lastly, intestinal CD4(+) T cells isolated from IBD patients responsive to treatment with antibodies against tumor necrosis factor-α (anti-TNF-α), the most effective known IBD therapy, exhibited reduced amounts of IL-22BP expression but still expressed IL-22. Our findings suggest that anti-TNF-α therapy may act at least in part by suppressing IL-22BP and point toward a more specific potential therapy for IBD.
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- info:eu-repo/semantics/restrictedAccess
- Quellsystem:
- Forschungsinformationssystem des UKE
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- Quelldatensatz
- oai:pure.atira.dk:publications/69256d34-5e37-421e-86b8-168dd45e84f5