Journal
AGING CELL
Volume 17, Issue 1, Pages -Publisher
WILEY
DOI: 10.1111/acel.12675
Keywords
aging; cytokine; inflammation; microarray; SASP; T cell
Categories
Funding
- British Heart Foundation
- Academy of Medical Science
- Wellcome trust
- William Harvey Research Foundation
- Medical Research Council
- British Biotechnology and Biological Research Council
- Academy of Medical Sciences (AMS) [SBF001\\1013] Funding Source: researchfish
- Biotechnology and Biological Sciences Research Council [BBS/B/04528, BB/L005336/1, BB/J006750/1] Funding Source: researchfish
- Medical Research Council [MR/M003833/1, MR/P00184X/1] Funding Source: researchfish
- BBSRC [BB/J006750/1, BB/L005336/1] Funding Source: UKRI
- MRC [MR/P00184X/1, MR/M003833/1] Funding Source: UKRI
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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 naive 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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