Chronic inflammation and aging: DNA damage tips the balance

Mary M. Cavanagh, Cornelia M. Weyand, Jörg J. Goronzy

Research output: Contribution to journalReview articlepeer-review

52 Scopus citations

Abstract

The aged immune system, typically hyporesponsive to infection and vaccination, can be hyperresponsive in the context of inflammatory pathology. Here we review current work examining the mechanisms behind the amplified inflammatory profile of aged adaptive immunity, and the reciprocal relationship between chronic inflammation and immune aging. Aged hematopoietic stem cells are driven to differentiate following accumulated DNA damage, thus depleting the stem cell pool and increasing the number of damaged effector cells in the circulation. Chronic DNA damage responses in lymphocytes as well as senescent cells of other lineages initiate the production of inflammatory mediators. In addition, aged lymphocytes become less reliant on specific antigen for stimulation and more prone to activation through innate receptors. When these lymphocytes are exposed to inflammatory signals produced by senescent tissues, the bias toward inflammation exacerbates destruction without necessarily improving immunity.

Original languageEnglish (US)
Pages (from-to)488-493
Number of pages6
JournalCurrent Opinion in Immunology
Volume24
Issue number4
DOIs
StatePublished - Aug 2012

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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