The role of T lymphocytes in host responses to sublethal systemic infection with was evaluated by mAb depletion of CD4 and CD8 cells from BALB/c and CBA/CaH mice, which develop mild and severe tissue damage, respectively. Depletion of CD4 lymphocytes from BALB/c mice markedly increased tissue damage, but did not alter the course of infection. In CBA/CaH mice, depletion of CD4 cells abrogated tissue destruction in both brain and kidney at day 4 after infection, and significantly decreased fungal colonization in the brain. However, the severity of tissue lesions increased relative to controls from day 8 onwards. A small increase in tissue damage was evident in both mouse strains after depletion of CD8 cells. There were no major differences between days 4 and 8 after infection in cDNA cytokine profiles of CD4 lymphocytes from either BALB/c or CBA/CaH mice. After passive transfer into infected syngeneic recipients, spleen cells from infected CBA/CaH mice markedly increased tissue damage when compared to controls, and also caused a significant increase in fungal colonization in the brain. A similar transfer in BALB/c mice increased the number of inflammatory cells in and around the lesions, but had no effect on the fungal burden in brain and kidney. The data demonstrate that both CD4 and CD8 lymphocytes contribute to the reduction of tissue damage after systemic infection with , and that the development and expression of CD4 lymphocyte effector function is influenced by the genetic background of the mouse.


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