Immune injury in the lung is classically divided into types I-IV hyper
sensitivity, with the complement system being involved in types II and
III hypersensitivity. Anaphylaxis and asthma are generally considered
prototypes of type I hypersensitivity and hypersensitivity pneumoniti
s as an example of type III hypersensitivity in the lung. However, in
asthma, for example, increasing evidence indicates that in addition to
mast cells, T lymphocytes play an important role. Therefore, consider
ing asthma as strictly a type I mediated reaction is too simplistic. T
his report will review the evidence regarding the involvement of the c
omplement system and complement activation products in anaphylaxis, as
thma and immune complex disease in various experimental models of pulm
onary disease. Identification of the mediators responsible for the sym
ptoms may suggest rational targets for the continued development of ef
fective therapy to combat immune injury in the lung. (C) 1997 Elsevier
Science B.V.