Recently there has been renewed interest in the potential of antibody immunity for the prevention and therapy of human Cryptococcus neoformans infections. Historically, the role of antibody immunity in protection against C. neoformans has been controversial. Experiments with polyclonal sera have produced evidence for and against the importance of antibody immunity in host defence. However, three groups have now shown that administration of monoclonal antibody (mAb) to the C. neoformans capsular polysaccharide (CPS) can modify the course of infection in mice. The quantity, isotype, and specificity of mAb appear to be important parameters of antibody efficacy against C. neoformans. Protective and nonprotective mAbs to CPS have been identified, suggesting a possible explanation for the divergent results obtained with polyclonal preparations, which presumably contain both types of antibodies. mAb administration has been shown to prolong survival, decrease organ fungal burden, and reduce serum polysaccharide antigen. The mechanism(s) by which mAb modify the course of infection is uncertain. In vitro experiments strongly suggest that antibodies mediate protection by enhancing effector cell function. The combination of antibody and amphotericin B is more effective than either agent alone for the treatment of murine cryptococcosis. Human–mouse chimeric antibodies with activity against C. neoformans have been constructed that may have advantages over mouse mAbs for therapy of human infections. A highly immunogenic capsular polysaccharide–protein vaccine has been made that can elicit protective antibodies in mice. Antibody immunity can modify the course of infection to the benefit of the host and may be useful in the prevention and treatment of human cryptococcosis. Key words: antibody, Cryptococcus neoformans, macrophage, vaccine, AIDS.