B Cell Recognition of Hyphae TLR 2 Promotes IgG1 and IL-6 Secretion for T17 Differentiation.

is 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 T1 and T17 cells are important for antifungal responses, the role of B cells and antibodies in protection from infection is less well defined. In this study, we show that hyphae but not yeast, as well as fungal cell wall components, directly activate B cells MyD88 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 of MyD88 signaling is also essential for induction of IL-6 secretion by B cells, which promotes T17 polarization in T-B cell coculture experiments. B cells may thus be activated directly by in its invasive form, leading to production of antibodies and T cell help for fungal clearance.