Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5935132 | The American Journal of Pathology | 2011 | 9 Pages |
Abstract
B cells mediate multiple functions that influence immune and inflammatory responses. In mice, the addition of dextran sulfate sodium (DSS) to drinking water leads to immediate intestinal injury. Dextran sulfate sodium-induced intestinal injury serves as an experimental animal model for human ulcerative colitis. The contribution of B cells to DSS-induced intestinal injury is unclear. In this study, we show that DSS-induced intestinal injury was more severe in CD19-deficient (CD19â/â) mice than in wild-type mice. These inflammatory responses were negatively regulated by a unique IL-10-producing CD1dhiCD5+ regulatory B cell subset (B10 cells) that was absent in CD19â/â mice and represented only 1% to 2% of splenic B220+ cells in wild-type mice. Remarkably, adoptive transfer of these B10 cells from wild-type mice reduced inflammation in CD19â/â mice in an IL-10-dependent manner. These results demonstrate that IL-10 production from regulatory B10 cells regulates DSS-induced intestinal injury. These findings may provide new insights and therapeutic approaches for treating ulcerative colitis.
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Authors
Koichi Yanaba, Ayumi Yoshizaki, Yoshihide Asano, Takafumi Kadono, Thomas F. Tedder, Shinichi Sato,