E-cadherin marks a subset of inflammatory dendritic cells that promote T cell-mediated colitis.
Autor: | Siddiqui KR; Sir William Dunn School of Pathology, University of Oxford, OX1 3RE Oxford, UK., Laffont S, Powrie F |
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Jazyk: | angličtina |
Zdroj: | Immunity [Immunity] 2010 Apr 23; Vol. 32 (4), pp. 557-67. Date of Electronic Publication: 2010 Apr 15. |
DOI: | 10.1016/j.immuni.2010.03.017 |
Abstrakt: | 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. (Copyright 2010 Elsevier Inc. All rights reserved.) |
Databáze: | MEDLINE |
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