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Natural IgM-mediated innate autoimmunity: a new target for early intervention of ischemia-reperfusion injury.

机译:天然IgM介导的先天性自身免疫:早期干预缺血再灌注损伤的新目标。

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摘要

Recent studies showed that innate autoimmunity is an early mechanism for ischemia-reperfusion (I/R) injury. Results from different animal models showed that reperfusion of ischemic tissues elicits an acute inflammatory response involving a complement system, which is activated by autoreactive natural IgM. Moreover, ischemia-specific self-targets were identified. In contrast to the unsuccessful attempts in the past to treat I/R injury, targeting natural IgM-mediated innate autoimmunity may open a new avenue for early intervention.
机译:最近的研究表明,先天性自身免疫是缺血再灌注(I / R)损伤的早期机制。来自不同动物模型的结果表明,缺血组织的再灌注引发涉及补体系统的急性炎症反应,该补体系统由自身反应性天然IgM激活。此外,确定了缺血特异性自我靶标。与过去治疗I / R损伤的尝试不同,相反,靶向天然IgM介导的先天性自身免疫可能为早期干预开辟新的途径。

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