Another study evaluating a role of the Th17 pathway in VVC included an animal model in which mice treated with halofuginone, an inhibitor of Th17 differentiation, produced significantly less IL-17 by vaginal CD4+ T cells and resulted in exacerbated vaginal infection due to impaired production of antimicrobial peptides β-defensin (BD)-2 and BD-3 by vaginal epithelial cells [12]. Here, CD4 is linked to infective vaginitis.