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J. Virol., Mar 1997, 2518-2521, Vol 71, No. 3
Copyright © 1997, American Society for Microbiology

Modification of the Sendai virus-specific antibody and CD8+ T-cell responses in mice homozygous for disruption of the interleukin-4 gene

XY Mo, MY Sangster, RA Tripp and PC Doherty
Department of Immunology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA.

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.


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