Journal
AMERICAN JOURNAL OF PATHOLOGY
Volume 178, Issue 2, Pages 735-743Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.ajpath.2010.10.022
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Funding
- Nakatomi Foundation
- National Institutes of Health [AI 56363]
- Southeastern Regional Center of Excellence for Emerging Infections and Biodefense [U54 AI057157]
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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 (CD19(-/-)) mice than in wild-type mice. These inflammatory responses were negatively regulated by a unique IL-10-producing CD1d(hl)CD5(+) regulatory B cell subset (B10 cells) that was absent in CD19(-/-) 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 CD19(-/-) 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. (Am J Pathol 2011, 178:735-743; DOI: 10.1016/j.ajpath.2010.10.022)
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