The Role of TLR2/TLR4 Receptors in Host Genetic Susceptibility to Recurrent Vulvovaginitis

Vulvovaginal candidiasis (VVC) is a prevalent vaginal infection predominantly attributed to <i>Candida albicans</i>. A considerable proportion of women experience more than three episodes of VVC annually, a condition referred to as recurrent vulvovaginal candidiasis (RVVC). It is estimated that RVVC affects more than 130 million women globally each year and has a substantial negative impact on their quality of life, resulting in physical discomfort, psychological distress, and social stigma. Nevertheless, not all individuals who develop VVC progress to RVVC, suggesting that genetic variation may play a critical role in host susceptibility. The present review aims to evaluate the associations between genetic predispositions-specifically polymorphisms in Toll-like receptors 2 and 4 (TLR2, TLR4)-and RVVC. TLRs are essential for detecting pathogen-associated molecular patterns (PAMPs) and initiating immune responses. During RVVC episodes, <i>Candida</i> undergoes a reversible transition from the yeast form to the hyphal form, resulting in alterations in surface PAMPs, which are subsequently recognized by innate immune receptors expressed on vaginal epithelial cells. Polymorphisms in these receptors may modulate individual susceptibility to RVVC. This review examines the literature on the impact of specific polymorphisms in TLR2 and TLR4 on fungal recognition and infection. Furthermore, the interactions between TLRs and other elements of the innate immune system have also been explored. A deeper understanding of how genetic variability in immune receptors influences infection susceptibility could pave the way for personalized therapeutic strategies for RVVC, potentially involving immunomodulatory agents or antifungal treatments tailored to an individual's genetic profile.