Mechanisms of immunosenescence: Lessons from models of accelerated immune aging

Sabine Le Saux, Cornelia M. Weyand, Jörg J. Goronzy

Research output: Contribution to journalArticlepeer-review

51 Scopus citations

Abstract

With increasing age, the ability of the adaptive immune system to respond to vaccines and to protect from infection declines. In parallel, the production of inflammatory mediators increases. While cross-sectional studies have been successful in defining age-dependent immunological phenotypes, studies of accelerated immune aging in human subpopulations have been instrumental in obtaining mechanistic insights. The immune system depends on its regenerative capacity; however, the T cell repertoire, once established, is relatively robust to aging and only decompensates when additionally stressed. Such stressors include chronic infections such as CMV and HIV, even when viral replication is controlled, and autoimmune diseases. Reduced regenerative capacity, chronic immune activation in the absence of cell exhaustion, T cell memory inflation, and accumulation of highly potent effector T cells in these patients synergize to develop an immune phenotype that is characteristic of the elderly. Studies of accelerated immune aging in autoimmune diseases have identified an unexpected link to chronic DNA damage responses that are known to be important in aging, but so far had not been implicated in immune aging.

Original languageEnglish (US)
Pages (from-to)69-82
Number of pages14
JournalAnnals of the New York Academy of Sciences
Volume1247
Issue number1
DOIs
StatePublished - Jan 2012

Keywords

  • Autoimmunity
  • CMV
  • HIV
  • Immune aging
  • Latency
  • Thymic involution

ASJC Scopus subject areas

  • Neuroscience(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • History and Philosophy of Science

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