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Cited by 68T-cell and B-cell ImmunologyTelomeres, Telomerase, and SenescenceGenetics, Aging, and Longevity in Model Organisms

Decreased proliferative capacity and increased susceptibility to activation-induced cell death in late-passage human cd4+ tcr2+ cultured T cell clones

Pawelec, Graham, Sansom, David, Rehbein, Arnika, Adibzadeh, Medi, Beckman, Ian·1996·Experimental Gerontology
DOI 10.1016/s0531-5565(96)00097-6
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Abstract

The growth characteristics in vitro of interleukin 2 (IL 2)-dependent human CD4+ alpha beta-T cell receptor-positive helper T cell clones (TCC) were studied in relation to alterations in surface phenotype, cytokine responsiveness, and susceptibility to activation-induced cell death (AICD). TCC derived from peripheral blood T cells had finite lifespans averaging 33 population doublings (PD) with a recorded maximum lifespan of 80 PD (n = 208). First analyses of the TCC were undertaken at ca. 25 PD, at which time all cells of all TCC expressed high intensity CD45RO and low intensity CD45RA, as well as high intensity CD95 (fas) and MHC class II antigens. The expression of these molecules remained elevated throughout the proliferative lifespan of the clones, but for those TCC which were initially CD28+ (the majority), the density of expression of the latter was diminished in most late-passage clones. Concomitant with this, late-passage cells showed reduced responsiveness to CD28-mediated costimulation by CHO transfectants expressing human CD80 compared to early-passage cells. Additionally, the level of expression of IL 2R gamma c and IL 7R chains was commonly reduced, as was the response to IL 2 and IL 7. Despite unchanged levels of fas expression on TCC with time, late-passage cells were more susceptible to AICD than early, passage cells. These observations further document functional and phenotypic alterations in long-term cultured human T helper cells, which may be considered as biomarkers of immunosenescence. This may contribute to an improved understanding of the mechanisms underlying depressed T cell function in old age.

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Authors
Pawelec, G., Sansom, D., Rehbein, A., Adibzadeh, M., & Beckman, I.
Affiliations
  • University of Tübingen (DE)
  • Bath Institute for Rheumatic Diseases (GB)
  • Flinders Medical Centre (AU)
Corresponding author
Pawelec, Graham
ORCID
Venue
Experimental Gerontology
Publisher
Elsevier BV
Published
1996-11
Volume
31
Issue
6
Pages
655-668
ISSN
0531-5565 (ISSN-L)
DOI
10.1016/s0531-5565(96)00097-6
OpenAlex
W2045928865
Cited by
68
References
39
Citations by year
2026: 1 · 2021: 1 · 2019: 2 · 2018: 2 · 2017: 1 · 2016: 1 · 2015: 1 · 2014: 1 · 2013: 2
FWCI
1.82
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Experimental Gerontology (publishedVersion)
  • PubMed (publishedVersion)
  • UCL Discovery (University College London) (submittedVersion)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
  • Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
Keywords
activation-induced cell death, CD4+ T cell clones, T cell proliferation, immunosenescence, CD28 costimulation, CD80, CD45RA/CD45RO, Fas, IL-2 receptor gamma chain, IL-7 receptor, cytokine responsiveness, T cell lifespan, T helper cells, aging
MeSH terms
Animals, Antigen-Presenting Cells, Cricetinae, Humans, Lymphocyte Activation, Receptors, Antigen, T-Cell, T-Lymphocytes, CD4 Antigens, Immunophenotyping, Cytokines, CHO Cells, Cellular Senescence

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