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*
World Health Organization Immunology Research and Training Center, Institute of Biochemistry, University of Lausanne, Epalinges, Switzerland;
Institute of Microbiology, University of Lausanne, Lausanne, Switzerland,
Departments of Medicine and Microbiology/Immunology and the Howard Hughes Medical Institute, University of California, San Francisco, CA 94143; and
§
Department of Dermatology, Ludwig Maximilian University, Munich, Germany
In contrast to intact BALB/c mice, BALB/c mice rendered deficient
in Vß4+ CD4+ T cells develop a Th1 response
to infection with Leishmania major and are resistant.
Vß4-deficient BALB/c mice are unable to generate the early IL-4
transcription occurring in Vß4 V
8 CD4+ T cells of
BALB/c mice within 1 day of infection. Here we demonstrate that
treatment of Vß4-deficient BALB/c mice with IL-4 during the first
64 h after infection instructs Th2 cell development and
susceptibility to infection. The demonstrated inability of IL-4 to
reverse the resistant phenotype of BALB/c mice treated with
anti-CD4 mAb the day before infection suggest that these effects of
IL-4 require its interaction with CD4+ T cells. In contrast
to draining lymph node cells from BALB/c mice, cells from
Vß4-deficient BALB/c mice remain responsive to IL-12 following
infection. Strikingly, administration of IL-4 to Vß4-deficient BALB/c
mice renders their lymph node cells unresponsive to IL-12 by
down-regulating IL-12R ß2-chain expression. This study directly
demonstrates that in BALB/c mice IL-4 is necessary and sufficient to
initiate the molecular events steering Th2 cell maturation and
susceptibility to L. major.
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