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.
引用
收藏
页码:195 / 200
页数:6
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