Antimicrobial response of a T cell-deficient host to cytokine therapy: Effect of interferon-γ in experimental visceral Leishmaniasis in nude mice Academic Article uri icon


MeSH Major

  • CD4-Positive T-Lymphocytes
  • CD8-Positive T-Lymphocytes
  • Interferon-gamma
  • Leishmania donovani
  • Leishmaniasis, Visceral


  • To determine if interferon (IFN)-gamma can enhance intracellular antimicrobial defense in a T cell-deficient host, nude BALB/c mice were infected with Leishmania donovani and treated with IFN-gamma. IFN-gamma 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-gamma; treatment with T cell-regulated antileishmanial cytokines (interleukin-2, granulocyte-macrophage colony-stimulating factor, or tumor necrosis factor-alpha) could not substitute for T cells. NK cells played no apparent role. In reconstituted nude mice, the antileishmanial effect of IFN-gamma correlated with markedly enhanced mononuclear cell recruitment to infected liver foci. Thus, although IFN-gamma 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-gamma may prove useful in intracellular infections in the T cell-deficient host.

publication date

  • January 1995



  • Academic Article



  • eng

PubMed ID

  • 7751708

Additional Document Info

start page

  • 1309

end page

  • 16


  • 171


  • 5