The senescence-accelerated mouse shows aging-related defects in cellular but not humoral immunity against influenza virus infection.
The senescence-accelerated mouse (SAM) strain P1, which has a short life span, was adopted as a murine model for an investigation of the pathogenesis of viral infection in elderly adults. After intranasal inoculation with influenza A virus, the SAM-P1 mice showed a higher rate of mortality, with prolonged virus growth in the lungs. The increased susceptibility was associated with impaired activity of both NK cells and virus-specific cytotoxic T lymphocytes. The production of interferon-gamma and interleukin-12 was significantly restrained, which suggests a partial deficiency of the T helper (Th) 1 cells. In contrast, the immunologic activity of the Th2 cells appeared to be functionally normal, judging from the release of large amounts of interleukin-4 followed by production of appropriate amounts of influenza virus-specific antibody. It is suggested that the elicitation of cellular immunity is an important and effective procedure for protecting the elderly from influenza virus infection.
Department of Microbiology, Fukui Medical University School of Medicine, Fukui, Japan.
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L
Dong
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Mori
M J
MJ
Hossain
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Y
Kimura
D000375:Aging / Q000276:immunology*; D000818:Animals; D000917:Antibody Formation; D016516:CD4-CD8 Ratio; D016207:Cytokines / Q000096:biosynthesis; D004198:Disease Susceptibility; D007111:Immunity, Cellular; D009980:Influenza A virus / Q000276:immunology*; D007694:Killer Cells, Natural / Q000276:immunology; D051379:Mice; D008806:Mice, Inbred AKR; D009976:Orthomyxoviridae Infections / Q000276:immunology*; D013154:Spleen / Q000166:cytology / Q000276:immunology; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology; D018417:Th1 Cells / Q000276:immunology; D013950:Thymus Gland / Q000166:cytology / Q000276:immunology
D016207:Cytokines