Key result
Complement and immune complexes drive reperfusion injury via neoantigen exposure and natural IgM activation.
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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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Chan et al. (2003) conducted a review in Reperfusion injury. Immune complexes and complement was evaluated on Mechanism of reperfusion injury. Complement and immune complexes act as critical players in mediating reperfusion injury through neoantigen expression, natural IgM trapping, and complement activation.
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