Immunity in vaginal candidiasis

Abstract

Vulvovaginal candidiasis and recurrent vulvovaginal candidiasis remain a significant problem in women of child-bearing age. While host defense mechanisms against infection are poorly understood, the most recent studies continue to challenge dogma relative to anti-Candida immunity at other mucosal sites that is normally associated with T helper 1-type CD4 T cells. Four studies comprise the latest findings in host defense against vulvovaginal candidiasis. The first from an animal model provided the most definitive data to date for the lack of involvement by systemic or local T-cell-mediated immunity. The second study confirmed a limited role for antibodies in vaginal candidiasis; similar to past studies, systemic and local Candida-specific antibodies in women with vulvovaginal candidiasis were either similar or elevated compared with controls. The third study from a cohort of adolescents provided evidence for some form of local protective immunity based on high asymptomatic vaginal fungal burden with low incidence rate of vulvovaginal candidiasis. This was addressed more specifically through a natural history protocol involving an intravaginal challenge with live Candida. Results showed a strong correlation between infiltration of polymorphonuclear neutrophils and symptomatic vulvovaginal candidiasis, with no evidence of an inflammatory response in those protected against infection. Instead of vulvovaginal candidiasis being caused by defective or dysfunctional CD4 T helper 1-type cell-mediated immune reactivity, data suggest that symptomatic vulvovaginal candidiasis is associated with an aggressive response by polymorphonuclear neutrophils, whereas protection appears to be innate and noninflammatory. The role for innate immunity in both protection against, and promotion of, symptomatic vulvovaginal candidiasis is paradigm changing.