Abstract
IL-19, a member of the IL-10 cytokine family that signals through the IL-20 receptor type I (IL-20Rα:IL-20Rβ), is a cytokine whose function is not completely known. In this article, we show that the expression of IL19 in biopsies of patients with active ulcerative colitis was increased compared with patients with quiescent ulcerative colitis and that colitis was attenuated in IL-19-deficient mice. The disruption of the epithelial barrier with dextran sodium sulfate leads to increased IL-19 expression. Attenuated colitis in IL-19-deficient animals was associated with reduced numbers of IL-6-producing macrophages in the inflamed colonic lamina propria. Microbial-driven expression of IL-19 by intestinal macrophages may contribute to the pathogenesis of inflammatory bowel disease.
Copyright © 2017 by The American Association of Immunologists, Inc.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Biopsy
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Colitis / immunology
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Colitis, Ulcerative / immunology*
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Colitis, Ulcerative / pathology
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Dextran Sulfate / administration & dosage
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Disease Models, Animal
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Humans
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Inflammatory Bowel Diseases / immunology*
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Inflammatory Bowel Diseases / pathology
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Interleukin-10 / deficiency
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Interleukin-10 / genetics*
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Interleukin-10 / immunology
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Interleukin-10 / metabolism
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Interleukin-6 / biosynthesis
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Interleukin-6 / immunology
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Interleukins / genetics*
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Interleukins / immunology
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Interleukins / metabolism
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Intestines / cytology
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Intestines / immunology
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Intestines / pathology
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Ligands
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Macrophages
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Mice
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Mucous Membrane / immunology
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Signal Transduction
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Toll-Like Receptors / immunology*
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Toll-Like Receptors / metabolism
Substances
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IL19 protein, human
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Il19 protein, mouse
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Interleukin-6
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Interleukins
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Ligands
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Toll-Like Receptors
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Interleukin-10
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Dextran Sulfate