Nathan Shock Memorial Lecture 1992. Aging and immune function: cellular and biochemical analyses.
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.
Miller
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Department of Pathology, University of Michigan Medical School, Ann Arbor 48109.
D000375:Aging / Q000276:immunology*; D000818:Animals; D002118:Calcium / Q000502:physiology; D003208:Concanavalin A / Q000494:pharmacology; D007153:Immunologic Deficiency Syndromes / Q000503:physiopathology; D007156:Immunologic Memory; D007376:Interleukin-2 / Q000494:pharmacology; D015759:Ionomycin / Q000494:pharmacology; D008213:Lymphocyte Activation; D051379:Mice; D011494:Protein Kinases / Q000502:physiology; D011505:Protein-Tyrosine Kinases / Q000502:physiology; D015398:Signal Transduction; D016176:T-Lymphocyte Subsets / Q000187:drug effects / Q000276:immunology*; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology
D007376:Interleukin-2; D003208:Concanavalin A; D015759:Ionomycin; D011494:Protein Kinases; D011505:Protein-Tyrosine Kinases; D013755:Tetradecanoylphorbol Acetate; D002118:Calcium