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

Exp Gerontol. Jan-Feb 1994;29(1):21-35. doi: 10.1016/0531-5565(94)90060-4.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Aging / immunology*
  • Animals
  • Calcium / physiology
  • Concanavalin A / pharmacology
  • Immunologic Deficiency Syndromes / physiopathology
  • Immunologic Memory
  • Interleukin-2 / pharmacology
  • Ionomycin / pharmacology
  • Lymphocyte Activation
  • Mice
  • Protein Kinases / physiology
  • Protein-Tyrosine Kinases / physiology
  • Signal Transduction*
  • T-Lymphocyte Subsets / drug effects
  • T-Lymphocyte Subsets / immunology*
  • Tetradecanoylphorbol Acetate / pharmacology

Substances

  • Interleukin-2
  • Concanavalin A
  • Ionomycin
  • Protein Kinases
  • Protein-Tyrosine Kinases
  • Tetradecanoylphorbol Acetate
  • Calcium