BIOCOMPATIBILITY - COMPLEMENT AS MEDIATOR OF TISSUE-DAMAGE AND AS INDICATOR OF INCOMPATIBILITY

Authors
Citation
Te. Mollnes, BIOCOMPATIBILITY - COMPLEMENT AS MEDIATOR OF TISSUE-DAMAGE AND AS INDICATOR OF INCOMPATIBILITY, Experimental and clinical immunogenetics, 14(1), 1997, pp. 24-29
Citations number
26
Categorie Soggetti
Genetics & Heredity",Immunology,Biology
ISSN journal
02549670
Volume
14
Issue
1
Year of publication
1997
Pages
24 - 29
Database
ISI
SICI code
0254-9670(1997)14:1<24:B-CAMO>2.0.ZU;2-E
Abstract
The fully biocompatible surface is the host's own intact endothelium. Blood contact with a damaged or foreign endothelium, or with an artifi cial surface, will lead to a certain degree of activation of the defen se systems. Complement is one of these systems which has a unique prop erty to distinguish between 'self' and 'non-self'. Recent data using c omplement-specific inhibitors like soluble CR1 and monoclonal antibodi es to C5 have shown that complement is not only associated with, but i n fact contributes to, the whole body inflammatory reaction seen as a complication to cardiopulmonary bypass (artificial surfaces) and is re sponsible for the hyperacute rejection of xenografts (foreign endothel ium). Complement activation, as measured by assays specific for neoepi topes exposed in the activation products, is a sensitive indicator of bioincompatibility. These assays have been increasingly important afte r a causal link between complement activation and tissue damage was de monstrated. Efforts have been made to improve the biocompatibility of artificial surfaces, including coating with heparin. This procedure no t only improves coagulation compatibility, but also markedly reduces c omplement activation. Models to study complement compatibility in vitr o and in vivo are described, and recommended complement activation ass ays reviewed.