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• W4313347866 endingPage "2894" @default.
• W4313347866 startingPage "2890" @default.
• W4313347866 abstract "Abstract Host defenses against infection are profoundly compromised in HIV-infected hosts due to progressive depletion of CD4+ T lymphocytes and defective cell-mediated immunity. Although recent advances in antiretroviral therapy can dramatically lower HIV viral load, blood CD4+ T lymphocytes are not restored to normal levels. Therefore, we investigated mechanisms of host defense other than those involving CD4+ T lymphocytes against a common HIV-related opportunistic infection, Pneumocystis carinii (PC) pneumonia. Using CD4-depleted mice, which are permissive for chronic PC infection, we show that up-regulation of murine IFN-γ by gene transfer into the lung tissue results in clearance of PC from the lungs in the absence of CD4+ lymphocytes. This resolution of infection was associated with a &gt;4-fold increase in recruited CD8+ T lymphocytes and NK cells into the lungs. The role of CD8+ T cells as effector cells in this model was further confirmed by a lack of an effect of IFN-γ gene transfer in scid mice or mice depleted of both CD4+ and CD8+ T cells. Cytokine mRNA analysis revealed that recruited, lung-derived CD8+ T cells had greater expression of IFN-γ message in animals treated with the IFN-γ gene. These results indicate that CD8+ T cells are capable of clearing PC pneumonia in the absence of CD4+ T cells and that this host defense function of CD8+ T cells, as well as their cytokine repertoire, can be up-regulated through cytokine gene transfer." @default.
• W4313347866 created "2023-01-06" @default.
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• W4313347866 date "1999-03-01" @default.
• W4313347866 modified "2023-10-17" @default.
• W4313347866 title "IFN-γ and CD8+ T Cells Restore Host Defenses Against<i>Pneumocystis carinii</i>in Mice Depleted of CD4+ T Cells" @default.
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• W4313347866 doi "https://doi.org/10.4049/jimmunol.162.5.2890" @default.
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