Abstract
We explored the physiological role of conventional dendritic cells (cDCs) in acute colitis induced by a single cycle of dextran sodium sulfate administration. Depending on their mode of activation and independently of T cells, cDCs can enhance or attenuate the severity of dextran sodium sulfate-induced colitis. The latter beneficial effect was achieved, in part, by IFN-1 induced by Toll-like receptor 9-activated cDCs. IFN-1 inhibits colonic inflammation by regulating neutrophil and monocyte trafficking to the inflamed colon and restraining the inflammatory products of tissue macrophages. These data highlight a novel role of cDCs in the regulation of other innate immune cells and position them as major players in acute colonic inflammation.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Acute Disease
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Adoptive Transfer
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Animals
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Colitis / chemically induced
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Colitis / immunology*
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Colitis / pathology
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Cytokines / metabolism
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Dendritic Cells / drug effects
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Dendritic Cells / immunology*
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Dextran Sulfate / administration & dosage
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Dextran Sulfate / pharmacology
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Diphtheria Toxin / pharmacology
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Down-Regulation / drug effects
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Drug Administration Schedule
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Inflammation Mediators / metabolism
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Interferon-beta / pharmacology
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Interleukin-10 / pharmacology
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Ligands
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Macrophages / drug effects
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Macrophages / immunology
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Mice
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Mice, Transgenic
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Phenotype
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Recombinant Proteins / pharmacology
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T-Lymphocytes / drug effects
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T-Lymphocytes / immunology*
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Toll-Like Receptor 9 / metabolism
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Treatment Outcome
Substances
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Cytokines
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Diphtheria Toxin
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Inflammation Mediators
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Ligands
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Recombinant Proteins
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Toll-Like Receptor 9
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Interleukin-10
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Interferon-beta
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Dextran Sulfate