共 20 条
B cells contribute to ischemia/reperfusion-mediated tissue injury
被引:37
作者:
Chen, Jie
[1
]
Crispin, Jose C.
[1
]
Tedder, Thomas F.
[2
]
Lucca, Jurandir Dalle
[3
]
Tsokos, George C.
[1
]
机构:
[1] Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Div Rheumatol, Boston, MA 02115 USA
[2] Duke Univ, Med Ctr, Dept Immunol, Durham, NC USA
[3] Walter Reed Army Inst Res, Dept Cellular Injury, Silver Spring, MD USA
关键词:
B cell;
CXCL13;
Inflammation;
Ischemia/reperfusion;
REPERFUSION INJURY;
ISCHEMIA-REPERFUSION;
CD20;
IMMUNOTHERAPY;
T-CELL;
COMPLEMENT;
MICE;
DEPLETION;
ANTIBODY;
AUTOIMMUNITY;
CXCL13;
D O I:
10.1016/j.jaut.2009.02.021
中图分类号:
R392 [医学免疫学];
Q939.91 [免疫学];
学科分类号:
100102 ;
摘要:
Multiple elements are known to participate in ischemia/reperfusion (I/R)-mediated tissue injury. Amongst them, B cells have been shown to contribute by the production of antibodies that bind to ischemic cells and fix complement. It is currently unknown whether B cells participate through antibody-independent mechanisms in the pathogenesis of I/R. In a mesenteric I/R model we found that B cells infiltrate the injured intestine of normal and autoimmune mice 2 h after reperfusion is established. B cell depletion protected mice from the development of I/R-mediated intestinal damage. The protection conferred by B cell depletion was significantly greater in MRL/lpr mice. Finally, we show that ischemic tissue expressed the B cell-attractant CXCL13 and infiltrating B cells expressed the corresponding receptor CXCR5. Our data grant B cells an antibody-independent role in the pathogenesis of intestinal I/R and suggest that B cells accumulate in the injured tissue in response to the chemokine CXCL13. (C) 2009 Elsevier Ltd. All rights reserved.
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页码:195 / 200
页数:6
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