Te. Mollnes, BIOCOMPATIBILITY - COMPLEMENT AS MEDIATOR OF TISSUE-DAMAGE AND AS INDICATOR OF INCOMPATIBILITY, Experimental and clinical immunogenetics, 14(1), 1997, pp. 24-29
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.