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

Journal

BRITISH JOURNAL OF SURGERY
Volume 90, Issue 12, Pages 1470-1478

Publisher

WILEY
DOI: 10.1002/bjs.4408

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Funding

  1. NIGMS NIH HHS [P50 GM 52585] Funding Source: Medline

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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.

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