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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




Journal article



Publication Date





557 - 567


Sir William Dunn School of Pathology, University of Oxford, OX1 3RE Oxford, UK.


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