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* Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine,
Immunology Graduate Program, and
Department of Microbiology and Immunology, University of Michigan, Ann Arbor, MI 48109
Immunity to the opportunistic fungus Cryptococcus neoformans is dependent on cell-mediated immunity. Individuals with defects in cellular immunity, CD4+ T cells in particular, are susceptible to infection with this pathogen. In host defense against a number of pathogens, CD8+ T cell responses are dependent upon CD4+ T cell help. The goal of these studies was to determine whether CD4+ T cells are required for the generation of antifungal CD8+ T cell effectors during pulmonary C. neoformans infection. Using a murine intratracheal infection model, our results demonstrated that CD4+ T cells were not required for the expansion and trafficking of CD8+ T cells to the site of infection. CD4+ T cells were also not required for the generation of IFN-
-producing CD8+ T cell effectors in the lungs. In CD4– mice, depletion of CD8+ T cells resulted in increased intracellular infection of pulmonary macrophages by C. neoformans, increasing the pulmonary burden of the infection. Neutralization of IFN- in CD4–CD8+ mice similarly increased macrophage infection by C. neoformans, thereby blocking the protection provided by CD8+ T cells. Altogether, these data support the hypothesis that effector CD8+ T cell function is independent of CD4+ T cells and that IFN- production from CD8+ T cells plays a role in controlling C. neoformans by limiting survival of C. neoformans within macrophages.
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