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Dendritic cells (DCs) play a pivotal role in controlling the balance between tolerance and immunity in the intestine. Gut conditioned CD103(+) DCs promote regulatory T (Treg) cell responses; however, little is known about DCs that drive inflammation in the intestine. Here, we show that monocyte-derived inflammatory DCs that express E-cadherin, the receptor for CD103, promote intestinal inflammation. E-cadherin(+) DCs accumulated in the inflamed mesenteric lymph nodes and colon, had high expression of toll-like receptors, and produced colitogenic cytokines, such as IL-6 and IL-23, after activation. Importantly, adoptive transfer of E-cadherin(+) DCs into T cell-restored immunodeficient hosts increased Th17 cell responses in the intestine and led to exacerbation of colitis. These results identify a monocyte-derived inflammatory DC subset that is associated with the pathogenesis of intestinal inflammation, providing a therapeutic target for the treatment of inflammatory bowel disease.

Original publication

DOI

10.1016/j.immuni.2010.03.017

Type

Journal article

Journal

Immunity

Publication Date

23/04/2010

Volume

32

Pages

557 - 567

Keywords

Animals, Antigens, CD, Antigens, CD11c, Cadherins, Cell Differentiation, Cell Movement, Colitis, Dendritic Cells, Gene Expression Regulation, Immunity, Innate, Inflammation, Integrin alpha Chains, Mice, Mice, Inbred BALB C, Monocytes, T-Lymphocytes