Fungi have been studied as prototype activators of tire complement cas
cade since the early 1900s. More recently attention has focused on the
role of the complement system in the pathogenesis of fungal infection
s. The interactions of Cryptococcus neoformans and Candida albicans wi
th the complement system are the most widely characterized; however, a
ll pathogenic fungi examined to date have the ability to initiate the
complement cascade. The molecular mechanisms for initiation and regula
tion of the complement cascade differ from one fungus to another, most
likely reflecting differences in the structure of the outer layers of
the cell wall. The molecular bases for such differences remain to be
identified. Studies of mycoses in experimental animals with induced or
congenital deficiencies in the complement system demonstrate that com
plement is an important inmate system for control of fungal infection.
Contributions to host resistance include opsonization and generation
of inflammatory mediators. Inflammation induced by chemotactic product
s of the complement system may contribute to tile pathogenesis of some
fungal infections.