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Human CD8+ EMRA T cells display a senescence-associated secretory phenotype regulated by p38 MAPK.

Authors
  • Callender, Lauren A1
  • Carroll, Elizabeth C1
  • Beal, Robert W J2
  • Chambers, Emma S3
  • Nourshargh, Sussan2
  • Akbar, Arne N3
  • Henson, Sian M1
  • 1 Translational Medicine and Therapeutics, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London, EC1M 6BQ, UK.
  • 2 Microvascular Research, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London, EC1M 6BQ, UK.
  • 3 Division of Infection and Immunity, University College London, London, WC1E 6JF, UK.
Type
Published Article
Journal
Aging cell
Publication Date
Oct 12, 2017
Identifiers
DOI: 10.1111/acel.12675
PMID: 29024417
Source
Medline
Keywords
License
Unknown

Abstract

Cellular senescence is accompanied by a senescence-associated secretory phenotype (SASP). We show here that primary human senescent CD8+ T cells also display a SASP comprising chemokines, cytokines and extracellular matrix remodelling proteases that are unique to this subset and contribute to age-associated inflammation. We found the CD8+ CD45RA+ CD27- EMRA subset to be the most heterogeneous, with a population aligning with the naïve T cells and another with a closer association to the effector memory subset. However, despite the differing processes that give rise to these senescent CD8+ T cells once generated, they both adopt a unique secretory profile with no commonality to any other subset, aligning more closely with senescence than quiescence. Furthermore, we also show that the SASP observed in senescent CD8+ T cells is governed by p38 MAPK signalling.

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