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The Journal of Immunology, 1998, 161: 6156-6163.
Copyright © 1998 by The American Association of Immunologists

The IL-4 Rapidly Produced in BALB/c Mice After Infection with Leishmania major Down-Regulates IL-12 Receptor ß2-Chain Expression on CD4+ T Cells Resulting in a State of Unresponsiveness to IL-121

Hayo Himmelrich, Carlos Parra-Lopez, Fabienne Tacchini-Cottier, Jacques A. Louis2 and Pascal Launois3

World Health Organization Immunology Research and Training Center, Institute of Biochemistry, University of Lausanne, Epalinges, Switzerland

Within 1 day of infection with Leishmania major, susceptible BALB/c mice produce a burst of IL-4 in their draining lymph nodes, resulting in a state of unresponsiveness to IL-12 in parasite-specific CD4+ T cells within 48 h. In this report we examined the molecular mechanism underlying this IL-12 unresponsiveness. Extinction of IL-12 signaling in BALB/c mice is due to a rapid down-regulation of IL-12R ß2-chain mRNA expression in CD4+ T cells. In contrast, IL-12R ß2-chain mRNA expression was maintained on CD4+ T cells from resistant C57BL/6 mice. The down-regulation of the IL-12R ß2-chain mRNA expression in BALB/c CD4+ T cells is a consequence of the early IL-4 production. In this murine model of infection, a strict correlation is shown in vivo between expression of the IL-12R ß2-chain in CD4+ T cells and the development of a Th1 response and down-regulation of the mRNA ß2-chain expression and the maturation of a Th2 response. Treatment of BALB/c mice with IFN-{gamma}, even when IL-4 has been produced for 48 h, resulted in maintenance of IL-12R ß2-chain mRNA expression and IL-12 responsiveness. The data presented here support the hypothesis that the genetically determined susceptibility of BALB/c mice to infection with L. major is primarily based on an up-regulation of IL-4 production, which secondarily induces extinction of IL-12 signaling.




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