Modification of the Sendai virus-specific antibody and CD8+ T-cell responses in mice homozygous for disruption of the interleukin-4 gene.
Homozygous disruption (-/-) of the interleukin-4 (IL-4) gene did not obviously modify the severity of Sendai virus infection in the highly susceptible 129/J mouse strain. The virus was cleared from the respiratory tract, and potent cytotoxic T lymphocyte (CTL) effectors were present in the cell population recovered by bronchoalveolar lavage. However, the prevalence of virus-specific CTL precursors (p) was consistently diminished in the spleen and regional lymph nodes of the IL-4 -/- mice at day 7 after infection. Also, virus-specific serum immunoglobulin G1 (IgG1) levels were greatly reduced and few IgG1-producing cells were detected in the lymphoid tissue. The effect on IgG1 class switching was to be expected, but the decrease in CTLp numbers has not been observed previously for a virus-specific immune response.
Mo
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Department of Immunology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA.
Sangster
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Tripp
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Doherty
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PC
D000818:Animals; D000914:Antibodies, Viral / Q000097:blood / Q000276:immunology*; D006720:Homozygote; D007074:Immunoglobulin G / Q000097:blood / Q000276:immunology; D015847:Interleukin-4 / Q000235:genetics*; D051379:Mice; D008810:Mice, Inbred C57BL; D018108:Respirovirus / Q000276:immunology*; D010253:Respirovirus Infections / Q000276:immunology*; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology*
D000914:Antibodies, Viral; D007074:Immunoglobulin G; D015847:Interleukin-4