Conventional dendritic cells regulate the outcome of colonic inflammation independently of T cells

Kazumichi Abe(University of California San Diego), Kim Nguyen(University of California San Diego), Sean Fine(University of California San Diego), Ji‐Hun Mo(University of California San Diego), Carol Shen(University of California San Diego), Steve Shenouda(University of California San Diego), Maripat Corr(University of California San Diego), Steffen Jung(Weizmann Institute of Science), Jong‐Dae Lee(University of California San Diego), Lars Eckmann(University of California San Diego), Eyal Raz(University of California San Diego)
Proceedings of the National Academy of Sciences
October 17, 2007
Cited by 115Open Access
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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.


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