ArticlePLoS biology2024
The dynamics and longevity of circulating CD4+ memory T cells depend on cell age and not the chronological age of the host.
Article in PLoS biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Frequency-selective thymic programming by early-life cold stress requires interferon regulatory factor 5.Frontiers in immunology · 2026Article
- Asynchronous aging and turnover of human circulating and tissue-resident memory T cells across sites.Immunity · 2025Article
- A variational deep-learning approach to modeling memory T cell dynamics.PLoS computational biology · 2025Article
- Tissue-resident memory CD4eLife · 2025Article
- A linear ontogeny accounts for the development of naive, memory, and tumor-infiltrating regulatory T cells in mice.Science immunology · 2025Article
- The impact of model assumptions in interpreting cell kinetic studies.PLoS computational biology · 2025Article
- A variational deep-learning approach to modeling memory T cell dynamics.bioRxiv : the preprint server for biology · 2025Article
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9 authors.
Funding
Abstract
Quantifying the kinetics with which memory T cell populations are generated and maintained is essential for identifying the determinants of the duration of immunity. The quality and persistence of circulating CD4 effector memory (TEM) and central memory (TCM) T cells in mice appear to shift with age, but it is unclear whether these changes are driven by the aging host environment, by cell age effects, or both. Here, we address these issues by combining DNA labelling methods, established fate-mapping systems, a novel reporter mouse strain, and mathematical models. Together, these allow us to quantify the dynamics of both young and established circulating memory CD4 T cell subsets, within both young and old mice. We show that that these cells and their descendents become more persistent the longer they reside within the TCM and TEM pools. This behaviour may limit memory CD4 T cell diversity by skewing TCR repertoires towards clones generated early in life, but may also compensate for functional defects in new memory cells generated in old age.
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