T-cell senescence: A culprit of immune abnormalities in chronic inflammation and persistent infection

Abbe N. Vallejo, Cornelia M. Weyand, Jörg J. Goronzy

Research output: Contribution to journalArticlepeer-review

167 Scopus citations

Abstract

Long-lived clonal T cells deficient in CD28 expression are commonly found in patients with inflammatory syndromes and persistent infections. Considering that CD28 loss is the most consistent immunological marker of aging, we propose that, in pathological states, CD28null T cells represent prematurely senescent cells resulting from persistent immune activation. These unusual lymphocytes have aberrant functions that contribute to disease-related immune abnormalities, and the degree of accumulation of CD28null T cells predicts the severity of clinical manifestations. We suggest that understanding of the biological properties of T cells that have reached replicative senescence will influence the future management of certain diseases. Indeed, studies on the molecular basis for the loss of CD28 are already providing information on methods to functionally rescue senescent T cells.

Original languageEnglish (US)
Pages (from-to)119-124
Number of pages6
JournalTrends in Molecular Medicine
Volume10
Issue number3
DOIs
StatePublished - Mar 2004

ASJC Scopus subject areas

  • Molecular Medicine
  • Molecular Biology

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