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

✍ Scribed by R. K. Chan; S. I. Ibrahim; N. Verna; M. Carroll; F. D. Moore Jr; H. B. Hechtman


Book ID
101749639
Publisher
John Wiley and Sons
Year
2003
Tongue
English
Weight
136 KB
Volume
90
Category
Article
ISSN
0007-1323

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✦ Synopsis


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.


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