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

Author:

Chan R K1,Ibrahim S I1,Verna N1,Carroll M1,Moore F D1,Hechtman H B1

Affiliation:

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

Abstract

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.

Funder

US Public Health Service

Trauma Research Foundation

Publisher

Oxford University Press (OUP)

Subject

Surgery

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