## Abstract ## Objective Collagen antibody–induced arthritis in mice exhibits a requirement for amplification by the alternative pathway of complement. Although the alternative pathway is activated by spontaneous hydrolysis, it is not known whether this pathway can also be initiated directly by Ig
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
- DOI
- 10.1002/bjs.4408
No coin nor oath required. For personal study only.
✦ 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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