Giant cell arteritis: Immune and vascular aging as disease risk factors

Shalini V. Mohan, Y. Joyce Liao, Jonathan W. Kim, Jörg J. Goronzy, Cornelia M. Weyand

Research output: Contribution to journalReview articlepeer-review

50 Scopus citations

Abstract

Susceptibility for giant cell arteritis increases with chronological age, in parallel with age-related restructuring of the immune system and age-induced remodeling of the vascular wall. Immunosenescence results in shrinkage of the naïve T-cell pool, contraction of T-cell diversity, and impairment of innate immunity. Aging of immunocompetent cells forces the host to take alternative routes for protective immunity and confers risk for pathogenic immunity that causes chronic inflammatory tissue damage. Dwindling immunocompetence is particularly relevant as the aging host is forced to cope with an ever growing infectious load. Immunosenescence coincides with vascular aging during which the arterial wall undergoes dramatic structural changes and medium and large arteries lose their pliability and elasticity. On the molecular level, elastic fibers deteriorate and matrix proteins accumulate biochemical modifications. Thus, the aging process impacts the two major biologic systems that liaise to promote giant cell arteritis; the immune system and the vessel wall niche.

Original languageEnglish (US)
Article number231
JournalArthritis Research and Therapy
Volume13
Issue number4
DOIs
StatePublished - Aug 2 2011

ASJC Scopus subject areas

  • Rheumatology
  • Immunology and Allergy
  • Immunology

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