High-dose intravenous immune globulin (IVIG) exerts a beneficial effec
t in a variety of immune disorders. One possible underlying mechanism
of this effect could be interference with the complement system. This
conclusion was based on the results obtained in animal models of compl
ement-mediated pathology, in vitro complement assays and studies on re
lated human diseases. Clearance of IgM-sensitized erythrocytes was spe
cifically suppressed by IVIG treatment. The same therapy prevented pul
monary endothelial cell lesions, the hallmark of Forssman shock, in 75
% of animals. All control animals, either untreated or injected with c
ontrol reagents, died within minutes following induction of Forssman s
hock. In vitro uptake of C3b and C4b complement fragments on to corpus
culate immune complexes was significantly inhibited by IVIG. Studies t
hat involved patients suffering from disorders with pathogenesis simil
ar to animal models of complement-mediated immune injury fully support
ed the hypothesis that IVIG interacts with activated complement compon
ents and prevents their deposition on target cells. The author's resul
ts suggest that IVIG can be an effective modulator of inappropriate co
mplement attack.