The Journal of Experimental Medicine
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Published 28 January 2002. doi:10.1084/jem.20011267
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© Rockefeller University Press, 0022-1007/2002/2/283/ $5.00
The Journal of Experimental Medicine, Volume 195, Number 3, February 4, 2002 283-293

Original Article

Aging Leads to Disturbed Homeostasis of Memory Phenotype CD8+ Cells

Xiaohong Zhang, Hideki Fujii, Hidehiro Kishimoto, Eric LeRoy, Charles D. Surh and Jonathan Sprent

Department of Immunology, IMM4 The Scripps Research Institute, La Jolla, CA 92037

Address correspondence to Jonathan Sprent, Dept. of Immunology, IMM4 The Scripps Research Institute, 10550 N. Torrey Pines Rd., La Jolla, CA 92037. Phone: 858-784-8619; Fax: 858-784-8839; E-mail: jsprent{at}scripps.edu

Examining the rate of in vivo T cell turnover (proliferation) in aged mice revealed a marked reduction in turnover at the level of memory-phenotype CD44hi CD8+ cells relative to young mice. Based on adoptive transfer experiments, the reduced turnover of aged CD44hi CD8+ cells reflected an inhibitory influence of the aged host environment. Aged CD44hi CD8+ cells also showed poor in vivo responses to IL-15 and IL-15–inducing agents, but responded well to IL-15 in vitro. Two mechanisms could account for the reduced turnover of aged CD44hi CD8+ cells in vivo. First, aging was associated with a prominent and selective increase in Bcl-2 expression in CD44hi CD8+ cells. Hence, the reduced turnover of aged CD44hi CD8+ cells may in part reflect the antiproliferative effect of enhanced Bcl-2 expression. Second, the impaired in vivo response of aged CD44hi CD8+ cells to IL-15 correlated with increased serum levels of type I interferons (IFN-I) and was largely reversed by injection of anti–IFN-I antibody. Hence the selective reduction in the turnover of aged CD44hi CD8+ cells in vivo may reflect the combined inhibitory effects of enhanced Bcl-2 expression and high IFN-I levels.

Key Words: aging • CD8+ cells • IFN-I • IL-15 • T cell turnover


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