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The Journal of Immunology, Vol 141, Issue 12 4209-4216, Copyright © 1988 by American Association of Immunologists

ARTICLES

Restricted expression of mitogen-induced high affinity IL-2 receptors in aging mice

JJ Proust, DS Kittur, MA Buchholz and AA Nordin
Clinical Immunology Section, National Institute on Aging, Baltimore, MD 21224.

Several lines of indirect evidence suggest that the number and/or affinity of IL-2R expressed by activated T lymphocytes declines with age and that this decline is implicated in the age-related proliferative impairment of Ag or mitogen-stimulated T cells. In an attempt to provide a direct demonstration of such a defect, various experimental approaches were used to analyze the expression of high and low affinity IL-2R as well as their functional properties in relation to age in purified populations of murine T lymphocytes. IL-2R were induced by Con A-activation which involves a transmembrane signaling mechanism or by exposure to phorbol dibutyrate (PDBu) which bypasses such a pathway. Consistent with the previously reported age-related defect in signal transduction, a major deficiency in the expression of high affinity IL-2R was observed in mitogen-activated cells derived from aged animals. As expected, PDBu-induction circumvented the transmembrane signaling defect and resulted in the restoration of a measurable amount of high affinity IL-2R expressed by cells from aged mice early after activation. The functional properties of the IL-2R expressed as a consequence of Con A or PDBu induction were investigated by assessing the proliferative response induced through the high affinity IL-2R as compared to that mediated by the beta-chain alone. Although Con A-induction resulted in a decreased expression of high affinity IL-2R by T lymphocytes derived from aged mice, the ability of these receptors as well as that of their beta-chain component to transmit a proliferative signal was identical in both age groups. In contrast, PDBu induced in both cell populations the expression of functionally aberrant IL-2R, unable to signal for proliferation unless excessively high concentrations of rIL-2 were available. The quantitative minimal estimate of the frequency of Con A-activated, IL-2- responsive cells showed a fourfold age-associated decrease, confirming the inability of a subpopulation of T lymphocytes from aged mice to express a sufficient density of high affinity IL-2R as a consequence of mitogenic activation.


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