Telomeres, immune aging and autoimmunity

Jörg J. Goronzy, Hiroshi Fujii, Cornelia M. Weyand

Research output: Contribution to journalReview articlepeer-review

80 Citations (Scopus)

Abstract

Telomere length is important in constraining the replicative potential of cells; cellular systems that are dependent on cell replenishment for renewal or on cell proliferation for functionality are highly sensitive to telomeric erosion. Cell replication invariably leads to telomere loss, which, in some cellular systems, is partially compensated for by telomerase activity. In addition to this typical telomere loss, several mechanisms of sporadic telomere loss exist. Heterogeneity in age-dependent telomere loss can be a consequence of increased cellular turnover during a lifetime, accelerated telomeric DNA damage, or defects in telomere repair. The immune system is a prime example of a highly dynamic cellular system, for which telomere maintenance is pivotal. Immune competence is strictly dependent on rapid expansions of clonal T- and B-cell populations, and telomere loss may contribute to defective immune responses in the elderly. Equally interestingly, accelerated T-cell aging combined with telomeric shortening may predispose for autoimmune responses and thereby explain the increased susceptibility for chronic inflammatory diseases in the elderly.

Original languageEnglish
Pages (from-to)246-251
Number of pages6
JournalExperimental Gerontology
Volume41
Issue number3
DOIs
Publication statusPublished - 2006 Mar
Externally publishedYes

Keywords

  • B cell
  • Immunosenescence
  • Premature aging syndrome
  • T cell
  • Telomerase
  • Telomere

ASJC Scopus subject areas

  • Biochemistry
  • Ageing
  • Molecular Biology
  • Genetics
  • Endocrinology
  • Cell Biology

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