Marked increase with age of type 1 cytokines within memory and effector/cytotoxic CD8+ T cells in humans: A contribution to understand the relationship between inflammation and immunosenescence

Franco Zanni, Rosanna Vescovini, Claudia Biasini, Francesco Fagnoni, Luca Zanlari, Annarita Telera, Patricia Di Pede, Giovanni Passeri, Mario Pedrazzoni, Mario Passeri, Claudio Franceschi, Paolo Sansoni

Research output: Contribution to journalArticle

Abstract

The ageing process is characterized by a progressive exhaustion of the naïve T cell reservoir that is accompanied by a compensatory expansion of effector/cytotoxic CD8+CD28- T cells. However, the origin and function of this subpopulation is not completely clarified. In this study, we examined the intracellular cytokine profile in purified CD8+ T cells obtained from 29 healthy subjects of different ages. Type 1 (IFN-γ IL-2 and TNF-α) and type 2 (IL-4, IL-6 and IL-10) cytokines were determined in three CD8+ T subsets, i.e. CD95-CD28 + (naïve), CD95+CD28- (effector/cytotoxic), and CD95+CD28+ (memory). As a general trend, we observed, in aged subjects, an increase of type 1 and type 2 intracellular cytokines within the three CD8+ subsets. In particular, we showed that type 1 cytokine-positive cells significantly increased, with age, among all the CD8+ subsets, while a marked increase of type 2 producing cells was observed only in memory CD8+ T cells. These profound changes are compatible with inflame-aging, an hypothesis which suggest that immunosenescence is mainly driven by a chronic antigenic load which not only induces an enormous expansion of CD28- T cells, but also increases their functional activity, exemplified by an high frequency of cells positive for pro-inflammatory cytokines.

Original languageEnglish
Pages (from-to)981-987
Number of pages7
JournalExperimental Gerontology
Volume38
Issue number9
DOIs
Publication statusPublished - Sep 1 2003

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Keywords

  • CD8 + T cells
  • Immunosenescence
  • Inflammation
  • Intracellular cytokines

ASJC Scopus subject areas

  • Ageing
  • Medicine(all)

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