B cell deficiency confers protection from renal ischemia reperfusion injury
B cell deficiency confers protection from renal ischemia reperfusion injury
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DOI：
10.4049/jimmunol.171.6.3210
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发表时间：
2003-09-15
影响因子：
4.4
通讯作者：
Rabb, H
中科院分区：
文献类型：
--
作者：
Burne-Taney, MJ;Ascon, DB;Rabb, H
最近的数据表明，CD4（+）细胞在肾缺血再灌注损伤（IRI）的发病机制中的作用。识别IRI中适应性免疫细胞的参与表明适应性免疫应答的另一个主要细胞，B细胞，也可能介导肾IRI。使用已建立的肾IRI模型：在B细胞缺陷（muMT）和野生型小鼠中进行肾蒂钳夹30分钟后再灌注。与野生型小鼠相比，muMT小鼠在缺血后24、48和72小时的肾功能显著改善。muMT小鼠还具有显著减少的肾小管损伤。通过髓过氧化物酶水平评估，两组小鼠缺血后肾脏吞噬细胞浸润相似，缺血后CD4（+）T细胞浸润水平相似。两组的管周补体C3d染色也相似。为了确定细胞与可溶性作用机制的贡献，血清转移到muMT小鼠中部分恢复了缺血表型，但B细胞转移没有。这些数据首次证明了B细胞在缺血性急性肾衰竭中的致病作用，血清因子是潜在的潜在作用机制。
Recent data have demonstrated a role for CD4(+) cells in the pathogenesis of renal ischemia reperfusion injury (IRI). Identifying engagement of adaptive immune cells in IRI suggests that the other major cell of the adaptive immune response, B cells, may also mediate renal IRI. An established model of renal IRI was used: 30 min of renal pedicle clamping was followed by reperfusion in B cell-deficient (muMT) and wild-type mice. Renal function was significantly improved in muMT mice compared with wild-type mice at 24, 48, and 72 h postischemia. muMT mice also had significantly reduced tubular injury. Both groups of mice had similar renal phagocyte infiltration postischemia assessed by myeloperoxidase levels and similar levels of CD4(+) T cell infiltration postischemia. Peritubular complement C3d staining was also similar in both groups. To identify the contribution of cellular vs soluble mechanism of action, serum transfer into muMT mice partially restored ischemic phenotype, but B cell transfers did not. These data are the first demonstration of a pathogenic role for B cells in ischemic acute renal failure, with a serum factor as a potential underlying mechanism of action.