B cell knockout mice are resistant to mucosal and systemic candidiasis of endogenous origin but susceptible to experimental systemic candidiasis.

Germfree J(H)D mice, which lack functional B cells and antibodies, were as resistant to orogastric and disseminated candidiasis of endogenous origin as were immunocompetent controls. Newborn J(H)D mice, in contrast to adult mice, were resistant to alimentary tract colonization by Candida albicans for 5-7 days after birth. C. albicans-colonized J(H)D mice were more resistant to intravenous challenge with C. albicans and had greater splenocyte proliferative responses to C. albicans antigens than did germfree mice or conventional controls. Thus, innate and acquired T cell-mediated immune responses induced after oral immunization are sufficient to protect J(H)D mice from mucosal and systemic candidiasis of endogenous origin; however, functional B cells may be required to protect mice from a primary intravenous challenge with C. albicans.