History and new insights into host defense against vaginal candidiasis

Recurrent vulvovaginal candidiasis (RVVC), caused by Candida albicans, remains a significant problem in women of childbearing age. Although cell-mediated immunity is considered the predominant host defense mechanism against mucosal candidal infections, two decades of research using animal models and results from clinical studies have revealed that adaptive immunity does not play a protective role against VVC owing to putative immunoregulatory mechanisms. Moreover, natural protective mechanisms and factors associated with susceptibility to infection have remained elusive until recently; use of a live challenge model in humans revealed that protection against vaginitis coincides with a non-inflammatory innate presence, whereas symptomatic infection correlates with a neutrophil infiltrate in the vaginal lumen and elevated fungal burden. Therefore, instead of RVVC being caused by a putative deficient adaptive immune response, it is now being considered that symptomatic vaginitis is caused by an aggressive innate response.