Underlying acquired immunity to the fungus Candida albicans is usually pres
ent in adult immunocompetent individuals and is presumed to prevent mucosal
colonization progressing to symptomatic infection. Exploration of immunolo
gical events leading to Candida resistance or susceptibility has indicated
the central role of the innate and adaptive immune systems, the relative co
ntribution of which may vary depending on the site of the primary infection
. Nevertheless, acquired resistance to infection results from the developme
nt of Th1 responses. Cytokines produced by Th1 cells activate phagocytic ce
lls to a candidacidal state. In contrast, cytokines produced by Th2 cells i
nhibit Th1 development and deactivate phagocytic effector cells. Because re
ciprocal influences have been recognized between innate and adaptive Th imm
unity, it appears that an integrated immune response determines the life-lo
ng commensalism of the fungus at the mucosal level, as well as the transiti
on from mucosal saprophyte to pathogen.