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An age-related decrease in rescue from T cell death following costimulation mediated by CD28

C R Engwerda1, B S Handwerger, B S Fox

  • 1Division of Rheumatology and Clinical Immunology, Department of Medicine, University of Maryland, Baltimore 21201, USA. c.engwerda@lshtm.ac.uk

Cellular Immunology
|May 25, 1996
PubMed
Summary
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T cell proliferation declines with age due to impaired response to costimulatory signals, not cytokine changes. Aged T cells fail to be rescued from cell death by CD28 costimulation, impacting immune function.

Area of Science:

  • Immunology
  • Aging Research
  • Cellular Immunology

Background:

  • T cell proliferation is crucial for adaptive immunity.
  • Previous work showed impaired T cell proliferation in aged mice.
  • The underlying mechanisms for this age-related defect require further investigation.

Purpose of the Study:

  • To investigate factors contributing to impaired T cell proliferation in aged mice.
  • To determine if altered cytokine production is responsible for the age-related defect.
  • To examine the role of CD28 costimulation in T cell survival and proliferation in aged mice.

Main Methods:

  • Splenic T cells from young and aged mice were stimulated with anti-CD3 epsilon and anti-CD28 antibodies.
  • Exogenous cytokines (IL-2, IL-4, IFN-gamma, IL-1 alpha, IL-6) were added to assess their impact on proliferation.

Related Experiment Videos

  • Cell cycle analysis was performed to evaluate cell division.
  • The protective effect of anti-CD28 costimulation against anti-CD3 epsilon-induced cell death was assessed.

    • Main Results:

    • Addition of exogenous cytokines did not improve the proliferative response of aged T cells.
    • Increased production of IFN-gamma or other inhibitory factors did not explain the reduced proliferation.
    • No significant difference in cell cycle progression was observed between young and aged T cells.
    • CD28 costimulation rescued young T cells from anti-CD3 epsilon-induced death, but failed to rescue aged T cells.

    Conclusions:

    • Impaired T cell response to CD28 costimulation contributes to reduced proliferation in aged mice.
    • This failure to respond to costimulatory signals may underlie various age-related immune dysfunctions.
    • Cytokine production changes are not the primary cause of the age-related T cell proliferation defect.