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IL-10-Producing Regulatory B10 Cells Inhibit Intestinal Injury in a Mouse Model
被引:132
作者:
Yanaba, Koichi
[2
]
Yoshizaki, Ayumi
[3
]
Asano, Yoshihide
Kadono, Takafumi
Tedder, Thomas F.
[4
]
Sato, Shinichi
[1
]
机构:
[1] Univ Tokyo, Fac Med, Dept Dermatol, Bunkyo Ku, Tokyo 1138655, Japan
[2] Jikei Univ, Sch Med, Dept Dermatol, Tokyo, Japan
[3] Nagasaki Univ, Grad Sch Biomed Sci, Dept Dermatol, Nagasaki 852, Japan
[4] Duke Univ, Med Ctr, Dept Immunol, Durham, NC USA
基金:
美国国家卫生研究院;
关键词:
B-LYMPHOCYTE DEPLETION;
EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS;
INFLAMMATORY-BOWEL-DISEASE;
ULCERATIVE-COLITIS;
T-CELLS;
B-1B CELLS;
MICE;
CD19;
ACTIVATION;
INITIATION;
D O I:
10.1016/j.ajpath.2010.10.022
中图分类号:
R36 [病理学];
学科分类号:
100104 ;
摘要:
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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页码:735 / 743
页数:9
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