CD4+ effector cells default to the Th2 pathway in interferon gamma-deficient mice infected with Leishmania major.

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  • Z E Wang
    Department of Medicine, University of California San Francisco 94143.
  • S L Reiner
    Department of Medicine, University of California San Francisco 94143.
  • S Zheng
    Department of Medicine, University of California San Francisco 94143.
  • D K Dalton
    Department of Medicine, University of California San Francisco 94143.
  • R M Locksley
    Department of Medicine, University of California San Francisco 94143.

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<jats:p>Mice with homologous disruption of the interferon gamma (IFN-gamma) gene on the C57BL/6 background were infected with Leishmania major and the immune response assessed. In contrast to wild-type or heterozygous knockout mice, deficient animals were unable to restrict growth of the parasite and suffered lethal infection over 6-8 wk. Although wild-type and heterozygous littermates developed CD4+ cells that contained transcripts for IFN-gamma and lymphotoxin, typical of T helper type 1 (Th1) cells, the knockout mice developed CD4+ cells that contained transcripts for interleukin 4 (IL-4), IL-5, and IL-13, typical of Th2 cells. ELISPOT assays confirmed the reciprocal patterns of IFN-gamma or IL-4 production by T cells in similar frequencies in the respective groups of mice, and antibody analysis confirmed the presence of Th2-mediated isotype switching in the knockout mice. These data suggest that CD4+ T cells that normally respond to antigens by differentiation to Th1 cells default to the Th2 pathway in the absence of endogenous IFN-gamma.</jats:p>

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