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缺血再灌注是一种由免疫复合物和补体引发的事件。

Ischaemia-reperfusion is an event triggered by immune complexes and complement.

作者信息

Chan R K, Ibrahim S I, Verna N, Carroll M, Moore F D, Hechtman H B

机构信息

Department of Surgery, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.

出版信息

Br J Surg. 2003 Dec;90(12):1470-8. doi: 10.1002/bjs.4408.

DOI:10.1002/bjs.4408
PMID:14648724
Abstract

BACKGROUND

Reperfusion injury is a common clinical problem that lacks effective therapy. Two decades of research implicating oxygen free radicals and neutrophils has not led to a single successful clinical trial.

METHODS

The aim was to review new clinical and preclinical data pertaining to the alleviation of reperfusion injury. A review of the literature was undertaken by searching the MEDLINE database for the period 1966-2003 without language restrictions.

RESULTS AND CONCLUSION

Evidence now points to complement and immune complexes as critical players in mediating reperfusion injury. Ischaemia is postulated to induce a phenotypical cellular change through the surface expression of a neoantigen. Preformed circulating natural IgM antibodies are then trapped and complement is activated. Final events leading to reperfusion injury include formation of the membrane attack complex and mast cell degranulation.

摘要

背景

再灌注损伤是一个缺乏有效治疗方法的常见临床问题。二十年来,涉及氧自由基和中性粒细胞的研究并未带来一项成功的临床试验。

方法

目的是回顾与减轻再灌注损伤相关的新临床和临床前数据。通过检索1966年至2003年期间的MEDLINE数据库进行文献综述,无语言限制。

结果与结论

现在有证据表明补体和免疫复合物是介导再灌注损伤的关键因素。据推测,缺血通过新抗原的表面表达诱导细胞表型改变。预先形成的循环天然IgM抗体随后被捕获,补体被激活。导致再灌注损伤的最终事件包括膜攻击复合物的形成和肥大细胞脱颗粒。

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Ischaemia-reperfusion is an event triggered by immune complexes and complement.缺血再灌注是一种由免疫复合物和补体引发的事件。
Br J Surg. 2003 Dec;90(12):1470-8. doi: 10.1002/bjs.4408.
2
A novel interpretation of immune redundancy and duality in reperfusion injury with important implications for intervention in ischaemic disease.对再灌注损伤中免疫冗余和二元性的一种新解释,对缺血性疾病的干预具有重要意义。
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Role of complement and perspectives for intervention in transplantation.补体在移植中的作用及干预策略。
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Ischemia/reperfusion injury: effect of simultaneous inhibition of plasma cascade systems versus specific complement inhibition.缺血/再灌注损伤:同时抑制血浆级联系统与特异性补体抑制的效果。
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Reperfusion syndrome: cellular mechanisms of microvascular dysfunction and potential therapeutic strategies.再灌注综合征:微血管功能障碍的细胞机制及潜在治疗策略
Vasc Endovascular Surg. 2007 Aug-Sep;41(4):277-93. doi: 10.1177/1538574407304510.
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[Pathophysiology of ischaemia-reperfusion injury].[缺血再灌注损伤的病理生理学]
Lijec Vjesn. 2006 Mar-Apr;128(3-4):87-95.
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The impact of ischaemia-reperfusion on the blood vessel.缺血再灌注对血管的影响。
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Marginal zone B cells transport and deposit IgM-containing immune complexes onto follicular dendritic cells.边缘区B细胞将含IgM的免疫复合物转运并沉积到滤泡树突状细胞上。
Int Immunol. 2004 Oct;16(10):1411-22. doi: 10.1093/intimm/dxh142. Epub 2004 Aug 23.
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Strategies for targeting complement inhibitors in ischaemia/reperfusion injury.针对缺血/再灌注损伤中补体抑制剂的策略。
Mol Immunol. 1999 Sep-Oct;36(13-14):957-63. doi: 10.1016/s0161-5890(99)00118-2.
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Natural antibody mediated innate autoimmune response.天然抗体介导的先天性自身免疫反应。
Mol Immunol. 2007 Jan;44(1-3):103-10. doi: 10.1016/j.molimm.2006.06.022. Epub 2006 Jul 28.

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