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Induction of inducible nitric oxide synthase in mononuclear phagocytes by IFN-γ and innate tumor necrosis factor (TNF) provide the basis for an effective immune response to the intracellular parasite  Leishmania (L.) major . In previous experiments, we observed a fatal visceral form of leishmaniasis in  L. major -infected C57BL/6 TNF -/-  mice. To further delineate the protective function of TNF and its receptor requirements, we comparatively assessed  L. major -infected C57BL/6 mice that were either deficient for membrane  and  soluble TNF ( Tnf  -   /   - ), for soluble TNF alone ( memTnf Δ/Δ  ), or the TNF receptors type 1 ( Tnfr1  -   /   - ) or type 2 ( Tnfr2  -   /   - ). We detected locally and systemically increased levels of the cytokine IFN-γ in the absence of the TNF-TNFR1-signaling pathway. An analysis of transcription factors and cytokines revealed that activated  Tnf  -   /   -  CD4 +  T cells displayed a highly active Th1 phenotype with a strong usage of the T cell receptor Vβ5.1/2. From these data we conclude that the fatal outcome of  L. major  infection in  Tnf  -   /   -  mice does not result from a skewed or deficient Th1 differentiation.

Fatal Leishmaniasis in the Absence of TNF Despite a Strong Th1 Response