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[Report] A pathogenic role for T cell–derived IL-22BP in inflammatory bowel disease

ScienceNOW - Fetched: October 20th, 2016, 3:00pm UTC

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. Authors: Penelope Pelczar, Mario Witkowski, Laura Garcia Perez, Jan Kempski, Anna G. Hammel, Leonie Brockmann, Dörte Kleinschmidt, Sandra Wende, Cathleen Haueis, Tanja Bedke, Marco Witkowski, Susanne Krasemann, Stefan Steurer, Carmen J. Booth, Philipp Busch, Alexandra König, Ursula Rauch, Daniel Benten, Jakob R. Izbicki, Thomas Rösch, Ansgar W. Lohse, Till Strowig, Nicola Gagliani, Richard A. Flavell, Samuel Huber

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