Immune aging and rheumatoid arthritis

Jorg J. Goronzy, Lan Shao, Cornelia M. Weyand

Research output: Contribution to journalReview articlepeer-review

55 Scopus citations

Abstract

Immunologic models of rheumatoid arthritis (RA) have to take into account that the disease occurs at an age when immunocompetence is declining and in a host whose immune system shows evidence of accelerated immune aging. By several immune aging biomarkers, the immune system in patients with RA is prematurely aged by more than 20 years. One major pathogenetic mechanism is a defect in telomere maintenance and DNA repair that causes accelerated cell death. These findings in RA are reminiscent of murine autoimmunity models, in which lymphopenia was identified as a major risk factor for autoimmunity. Progress in the understanding of how accelerated immune aging is pathogenetically involved in RA may allow development of new therapeutic approaches that go beyond the use of anti-inflammatory agents and eventually could open new avenues for preventive intervention.

Original languageEnglish (US)
Pages (from-to)297-310
Number of pages14
JournalRheumatic Disease Clinics of North America
Volume36
Issue number2
DOIs
StatePublished - May 2010

Keywords

  • Aging
  • Autoimmunity
  • Immunosenescence
  • Rheumatoid arthritis
  • Telomere

ASJC Scopus subject areas

  • Rheumatology

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