Candida albicans is a polymorphic fungus that colonizes mucosal tissue, and is thus a frequent member of the human microbiome. While it is no threat to healthy individuals, C. albicans can become pathogenic in immunocompromised hosts, being one of the most common human fungal pathogens, and one of the leading causes of nosocomial infections. For many years, and especially due to the fact that patients with B cell or immunoglobulin deficiencies do not show any increased propensity to C. albicans infections, B cells and antibodies were considered not to play any role in defensive responses against this pathogen. However, several studies have contradicted this view so that nowadays, even though not considered as major players like neutrophils or TH17 cells, B cells are seen as helpers in mounting efficient anti-C. albicans protective responses. To study the interplay between C. albicans and B cells, mouse splenic B cells were isolated and cultured in the presence of heat-killed C. albicans yeast, hyphae, or the fungal cell wall preparation zymosan. Cultures in unsupplemented medium or medium supplemented to mimic either T cell-independent or T-cell dependent B cell activation were analysed. The obtained results allowed to conclude that zymosan and heat-killed C. albicans hyphae, but not yeast, are able to increase B cell activation in a MyD88-dependent manner, and mostly via TLR2. This conclusion was drawn from the observed increase in AID induction and IgG1, IL-10 and IL-6 production. Dectin-1 and specific BCR recognition were not required for this effect. Furthermore, it was possible to observe that C. albicans-induced TLR signalling is able to cooperate with BCR signalling to increase B cell proliferation.