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Exp Gerontol. 1994 Jan-Feb;29(1):21-35.

Nathan Shock Memorial Lecture 1992. Aging and immune function: cellular and biochemical analyses.

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Department of Pathology, University of Michigan Medical School, Ann Arbor 48109.


Recent progress on the cellular and molecular basis for T cell dysfunction in aged mice is reviewed, with emphasis on defects in calcium signal generation and protein kinase function. The accumulation in older mice of memory T cells at the expense of naive T cells seems to account for most of the decline in the proportion of cells that can secrete or respond to interleukin 2. Memory T cells in mice of any age have an intrinsic resistance to increases in cytoplasmic free calcium ion concentration, which in turn interferes with their responses to polyclonal activators. T cells from old mice also exhibit declines both in serine/threonine and in tyrosine-specific protein kinase signals after activation by either receptor-dependent or receptor-independent agonists.

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