B cells contribute to ischemia/reperfusion-mediated tissue injury.

B cells contribute to ischemia/reperfusion-mediated tissue injury.
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DOI:
10.1016/j.jaut.2009.02.021
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发表时间:
2009-05
影响因子:
12.8
通讯作者:
Tsokos GC
Tsokos GC
中科院分区:
医学1区
文献类型:
--
作者:
Chen J;Crispín JC;Tedder TF;Dalle Lucca J;Tsokos GC

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已知多种元素参与缺血再灌注(I/R)介导的组织损伤。其中,B细胞已被证明通过产生与缺血细胞结合并固定补体的抗体而起作用。目前尚不清楚B细胞是否通过抗体非依赖性机制参与I/R的发病机制。在肠系膜I/R模型中,我们发现B细胞在建立再灌注后2小时浸润正常和自身免疫小鼠的损伤肠。B细胞耗竭保护小鼠免受I/R介导的肠损伤的发展。在MRL/lpr小鼠中,B细胞耗竭所赋予的保护作用显著更大。最后,我们发现缺血组织表达了B细胞吸引剂CXCL 13,浸润的B细胞表达了相应的受体CXCR 5。我们的数据赠款B细胞在肠I/R的发病机制中具有抗体非依赖性作用,并表明B细胞在响应趋化因子CXCL 13的损伤组织中积累。
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 hours 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 grants B cells an antibody-independent role in the pathogenesis of intestinal I/R and suggests that B cells accumulate in the injured tissue in response to the chemokine CXCL13.
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