Pathogenesis of Viral Pneumonia with Aging
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Following intranasal inoculation with respiratory viruses such as influenza virus and respiratory syncytial virus, the senescence-accelerated mouse strain P1 (SAM-P1) causes severe pneumonia, with elevated virus growth in the lung and prolonged virus shedding. The increased susceptibility to virus infection is associated with diminished cellular immunity by virus-specific cytotoxic T lymphocytes and natural killer cells and in part with the restrained production of virus-specific mucosal IgA antibody. The deficiency in cellular immune responses is due to a lack of clonal expansion of CD4^+ and CD8^+ T lymphocytes, together with an imbalance of T-helper type 1 (Th1) /Th2 cytokine production in the respiratory tract. The adoptive transfer of immune competent spleen cells from senescence-regular control mice and treatment with an immunostimulatory oligodeoxynucleotide containing a cytidine-guanosine motif achieve an appreciable protection for SAM-P1 mice.
- 岐阜医療科学大学の論文
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