Immunobiology of Aging*

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Abstract
Normal immune functions can begin to decline shortly after an individual reaches sexual maturity. Although changes in cellular environment are partially responsible, the decline is due primarily to changes within the cells, especially the T cells and to some extent the stem cells. This is reflected in their inability to proliferate and differentiate efficiently. What needs to be resolved is whether the altered properties of T cells and stem cells are permanent or reversible and, if permanent, whether they are due to a stochastic or a genetically programmed event. The decline with age in certain normal immune functions is associated with an increase in the frequency of autoimmune and immune complex diseases, certain types of cancer, and viral and fungal infections. These diseases compromise normal immune functions in short‐lived strains of mice. In long‐lived mice and in humans, however, the decline in immune functions to threshold levels seems to predispose in‐individuals to illness.Three general approaches recently have been used to improve the immune system of aging mice: a) dietary manipulation, b) drug therapy, and c) cellular therapy. Preliminary results of ongoing studies have been most encouraging. Future immu‐nopathogenic studies of aging mice with such an improved immune system should clarify the role of fidelity of the immune system in diseases of the aged. The immune system continues to serve as an excellent model for: a) the etiology of aging at the cellular and molecular levels, b) the pathogenesis of aging, and c) effective approaches to improve the quality of life for the aged.