Importance of beta(2)-microglobulin in murine resistance to mucosal and systemic candidiasis

beta(2)-Microglobulin knockout (beta 2m(-/-)) mice, which lack major histocompatibility complex class I expression and are deficient in CD8 alpha/beta T-cell receptor alpha/beta (TcR alpha/beta) T cells, were as resistant to systemic (intravenous) challenge with Candida albicans as immunocompetent controls. Conversely, the beta 2m(-/-) mutant mice were susceptible to systemic candidiasis of endogenous origin despite the induction of C. albicans-specific antibody and cell-mediated immune responses after colonization with a pure culture of C. albicans. Despite some superficial and transient infections of tongues and esophagi (detected by histology) at 1 to 2 weeks after oral colonization and gastric infections (cardia-antrum section) which were observed at 10 to 12 weeks after oral challenge, C. albicans-colonized beta 2m(-/-) mice showed an overall resistance to candidiasis in other mucosal and cutaneous tissues. These data suggest that immune defects that accompany the loss of beta(2)-microglobulin play an important role in murine resistance to gastric and disseminated candidiasis of endogenous (intestinal tract) origin and that innate immunity and CD4 TcR alpha/beta as well as CD8 alpha/alpha TcR alpha/beta> (or -gamma/delta) T cells play an important role in resistance to systemic, cutaneous, and nongastric mucosal tissues.