Antimicrobial Response of a T Cell-Deficient Host to Cytokine Therapy: Effect of Interferon- in Experimental Visceral Leishmaniasis in Nude Mice

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Abstract
To determine if interferon (IFN)-γ can enhance intracellular antimicrobial defense in a T cell-deficient host, nude BALB/c mice were infected with Leishmania donovani and treated with IFN-γ. IFN-γ induced killing of L. donovani in livers of euthymic mice but had no effect in nude mice despite activating peritoneal macrophages in vivo. Transfer of CD4+ or CD8+ T cells permitted nude mice to respond to IFN-γ; treatment with T cell-regulated antileishmanial cytokines (interleukin-2, granulocyte-macrophage colony-stimulating factor, or tumor necrosis factor-α) could not substitute for T cells. NK cells played no apparent role. In reconstituted nude mice, the antileishmanial effect of IFN-γ correlated with markedly enhanced mononuclear cell recruitment to infected liver foci. Thus, although IFN-γ activates macrophages in the absence of host T cells, a T cell mechanism is required for antileishmanial activity in tissue. Provided one T cell subset is adequately preserved, IFN-γ may prove useful in intracellular infections in the T cell-deficient host.

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