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• W1566301355 abstract "We have previously demonstrated that about 70% of elderly persons exhibit deficient cytotoxic T lymphocyte (CD8+ CTL) responses against influenza viruses when compared to young persons. Since IFN-γ, a Th1 cytokine and IL-4, a Th2 cytokine, stimulate and inhibit CD8+ CTL responses respectively, their role(s) in the age-related CTL deficiency was investigated. Lymphocytes from young adults (34±5 years old) and elderly subjects (71±1 years old) were stimulated in vitro with influenza A/H3N2, A/H1N1 or influenza B virus for 6–7 days. The CD8+ CTL activity against virus-infected autologous target cells was significantly lower among the elderly than the young subjects (P<0.01). Following stimulation with influenza virus, IL-4 production in both age groups was similar on day 3 but significantly higher among elderly persons on day 6 (P<0.05). In contrast, T cells from the elderly produced significantly lower IFN-γ than did those from young persons on both days (P<0.05). Treatment of T cells from young and elderly adults with recombinant human IL-12, a pivotal cytokine that stimulates Th1 cytokines, resulted in enhancement of CD8+ CTL activity and IFN-γ production in a dose dependent manner (P<0.01). IL-12-dependent enhancement of CTL activity was not always abrogated by anti-IFN-γ antibody treatment. These results suggest that deficient influenza virus-specific CTL activity among the elderly is attributable to a Th1 to Th2 cytokine production switch. Immunotherapy with IL-12 could represent a useful approach to correct the CD8+ CTL deficiency and cytokine imbalance among elderly humans." @default.
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• W1566301355 date "1997-03-01" @default.
• W1566301355 modified "2023-09-27" @default.
• W1566301355 title "Cytokines and impaired CD8+ CTL activity among elderly persons and the enhancing effect of IL-121This paper was presented at the First International Conference on Immunology and Aging, June 13–19, 1996, Bethesda, MD, USA.1" @default.
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• W1566301355 doi "https://doi.org/10.1016/s0047-6374(96)01855-6" @default.
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