Abstract
Despite extensive investigation, the mechanisms of host resistance against C. albicans infection remain poorly understood. Granulocytes and macrophages are the major effector cell types; however, their intrinsic candidacidal activity is rather limited, and its full expression requires augmentation by components of the T cell-initiated lymphokine cascade. Consequently, susceptibility to recurrent mucocutaneous infections may be associated with aberrant T cell function. In contrast, protection from systemic infection appears to be mediated by candida-specific antibodies.
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