Candida albicansis usually a benign member of the human gut microbiota, but can become pathogenic under certain circumstances, for example in an immunocompromised host. The innate immune system, in particular neutrophils and macrophages, constitutes a crucial first line of defense against fungal invasion, however adaptive immunity may provide long term protection and thus allow vaccination of at risk patients. While T_H1 and T_H17 cells are important for antifungal responses, the role of B cells and antibodies in protection fromC. albicansinfection is less well defined. In this study, we show thatC. albicanshyphae but not yeast, as well as fungal cell wall components, directly activate B cellsviaMyD88 signaling triggered by Toll- like receptor 2, leading to increased IgG1 production. While Dectin-1 signals and specific recognition by the B cell receptor are dispensable for B cell activation in this system, TLR2/MyD88 signals cooperate with CD40 signals in promoting B cell activation. Importantly, recognition ofC. albicans viaMyD88 signaling is also essential for induction of IL-6 secretion by B cells, which promotes T_H17 polarization in T-B cell coculture experiments. B cells may thus be activated directly byC. albicansin its invasive form, leading to production of antibodies and T cell help for fungal clearance.