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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Identification of a specific self-reactive IgM antibody that initiates intestinal ischemia/reperfusion injury
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Identification of a specific self-reactive IgM antibody that initiates intestinal ischemia/reperfusion injury

机译：鉴定引发肠道缺血/再灌注损伤的特异性自反应性IgM抗体

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摘要

Reperfusion injury of ischemic tissue represents an acute inflammatory response that can cause significant morbidity and mortality. The mechanism of injury is not fully elucidated, but recent studies indicate an important role for natural antibody and the classical pathway of complement. To test the hypothesis that injury is initiated by specific IgM, we have screened a panel of lgM-producing hybridomas prepared from peritoneal cells enriched in B-1 cells. One clone, CM22, was identified that could restore pathogenic injury in RAG-1(-/-) mice in an intestinal model of ischemia/reperfusion (I/R). In situ activation of the classical pathway of complement was evident by deposition of IgM, complement C4, and C3 in damaged tissue after passive transfer of CM22 IgM. Sequence analysis of CM22 Ig heavy and light chains showed germ-line configurations with high homology to a V-H sequence from the B-1 repertoire and a V-K of a known polyreactive natural IgM. These data provide definitive evidence that I/R injury can be initiated by clonally specific natural IgM that activates the classical pathway of complement. This finding opens an avenue for identification of I/R-specific self-antigen(s) and early prevention of injury. [References: 32]
机译：缺血组织的再灌注损伤代表一种急性炎症反应，可引起明显的发病率和死亡率。损伤的机制尚未完全阐明，但最近的研究表明天然抗体和经典补体途径的重要作用。为了检验由特定IgM引发损伤的假说，我们筛选了一组由富含B-1细胞的腹膜细胞制备的产生lgM的杂交瘤。在肠缺血/再灌注（I / R）肠道模型中，鉴定出一个克隆CM22，可以恢复RAG-1（-/-）小鼠的致病性损伤。在CM22 IgM被动转移后，IgM，补体C4和C3在受损组织中的沉积明显证明了补体经典途径的原位激活。 CM22 Ig重链和轻链的序列分析显示，与来自B-1库的V-H序列和已知的多反应性天然IgM的V-K具有高度同源性的种系构型。这些数据提供了明确的证据，表明I / R损伤可以通过激活补体经典途径的克隆特异性天然IgM引发。该发现为鉴定I / R特异性自身抗原和早期预防伤害开辟了道路。 [参考：32]

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