Abstract
Only during the past twenty years have attempts been made to carefully and systematically document declining function of the immunologic system with age. It is now known that senescence of the immunologic system occurs in all mammalian species studied, as measured by a variety of immunologic indices. Thus, amongst most but not all of the cellular components constituting the immune system, age dependent deficits in proliferation, differentiation and function have been found. For example, mitogenic responses of lymphocytes, ability of stem cells to reconstitute irradiated hosts, recognition of threshold doses of antigen, and maximum humoral antibody responses are all decreased with aging (Heidrick and Hakinodan, 1972a; Ram, 1967; Lajtha and Schofield, 1971). The consequences of this immunologic decline are very important to the organism and have been implicated in increased susceptibility of old animals to a variety of infectious insults and the increased incidence of neoplasia. General theories of aging have been postulated linking this decline in immunity, and an associated rise of autoimmunity, with most of the diseases attributed to the aging process including cancer and atherosclerosis (Walford, 1969, Robert and Robert, 1973). Since aging influences the differentiation and proliferation potential of immunologic cells, the immune system is an ideal model for the study of aging at the cellular level. Compelling reasons for this view are listed in Table I.
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Stoltzner, G., Makinodan, T. (1975). Age Dependent Decline in Proliferation of Lymphocytes. In: Cristofalo, V.J., Roberts, J., Adelman, R.C. (eds) Explorations in Aging. Advances in Experimental Medicine and Biology, vol 61. Springer, New York, NY. https://doi.org/10.1007/978-1-4615-9032-3_2
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