期刊
NATURE CELL BIOLOGY
卷 24, 期 10, 页码 1461-+出版社
NATURE PORTFOLIO
DOI: 10.1038/s41556-022-00991-z
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资金
- Wellcome Trust [110229/Z/15/Z]
- Italian Ministry of Health [GR-2018 12365916]
- Wellcome Trust Principal Research Fellowship [100262Z/12/Z]
- Kennedy Trust for Rheumatology Research
- Medical Research Council [MR/P00184X/1]
- NIH [R37AI04477]
- Wellcome Trust [110229/Z/15/Z] Funding Source: Wellcome Trust
It was discovered that some T cells can elongate telomeres by acquiring telomere vesicles from antigen-presenting cells, independently of telomerase action, which contributes to delaying the aging process.
The common view is that T lymphocytes activate telomerase to delay senescence. Here we show that some T cells (primarily naive and central memory cells) elongated telomeres by acquiring telomere vesicles from antigen-presenting cells (APCs) independently of telomerase action. Upon contact with these T cells, APCs degraded shelterin to donate telomeres, which were cleaved by the telomere trimming factor TZAP, and then transferred in extracellular vesicles at the immunological syn-apse. Telomere vesicles retained the Rad51 recombination factor that enabled telomere fusion with T-cell chromosome ends lengthening them by an average of similar to 3,000 base pairs. Thus, there are antigen-specific populations of T cells whose ageing fate decisions are based on telomere vesicle transfer upon initial contact with APCs. These telomere-acquiring T cells are protected from senescence before clonal division begins, conferring long-lasting immune protection.
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