An intercellular transfer of telomeres rescues T cells from senescence and promotes long-term immunological memory

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.

Automated summary

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.