Inflammatory cytokines overcome age-related defects in CD4 T cell responses in vivo

J Immunol. 2004 May 1;172(9):5194-9. doi: 10.4049/jimmunol.172.9.5194.

Abstract

Age-related decreases in immune function are thought to contribute to the reduced efficacy of vaccinations seen in elderly populations. Our previous in vitro studies demonstrated that naive CD4 T cells from aged TCR-transgenic mice proliferate less than young cells and generate poorly functioning effectors due to decreased IL-2 production. In this current study, we show that this age-related defect in CD4 T cell response also occurs in vivo and that it is correlated with reduced NF-kappa B activation. After transfer to young hosts, CD4 T cells from aged transgenic mice proliferate less and produce reduced levels of IL-2 upon immunization with Ag and alum. Introducing a combination of the inflammatory cytokines TNF-alpha, IL-1, and IL-6, or the use of an adjuvant such as CFA that induces these cytokines, markedly enhanced responses of these aged CD4 T cells, so that they proliferated and produced IL-2 similar to young cells. This enhancement is correlated with the enhanced activation of the transcription factor NF-kappa B in aged cells. We suggest that induction of inflammatory cytokines via adjuvants may enhance the efficacy of vaccinations in elderly populations.

Publication types

  • Comparative Study
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adoptive Transfer
  • Aging / genetics
  • Aging / immunology
  • Animals
  • CD4-Positive T-Lymphocytes / cytology*
  • CD4-Positive T-Lymphocytes / immunology*
  • CD4-Positive T-Lymphocytes / metabolism
  • CD4-Positive T-Lymphocytes / transplantation
  • Cell Division / genetics
  • Cell Division / immunology
  • Cells, Cultured
  • Cellular Senescence / genetics
  • Cellular Senescence / immunology*
  • Cytokines / administration & dosage
  • Cytokines / biosynthesis
  • Cytokines / physiology*
  • Down-Regulation / immunology
  • Immunophenotyping
  • Inflammation Mediators / administration & dosage
  • Inflammation Mediators / pharmacology*
  • Interleukin-2 / antagonists & inhibitors
  • Interleukin-2 / biosynthesis
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Mice, Transgenic
  • Peptides / administration & dosage
  • Peptides / immunology
  • Peptides / pharmacology
  • Transcription Factors / antagonists & inhibitors
  • Transcription Factors / biosynthesis
  • Transcription Factors / physiology

Substances

  • Cytokines
  • Inflammation Mediators
  • Interleukin-2
  • Peptides
  • Transcription Factors