What this means
Viral acute respiratory distress syndrome (ARDS) exhibits distinct clinical outcomes across age groups, but the immune mechanisms underlying this disparity remain unclear. Here, we integrated single-cell transcriptomic profiling, T cell receptor repertoire analysis, serum proteomics, and functional validation to characterize age-dependent T cell remodeling in influenza-associated ARDS.
A plain-English summary is on its way. Until then, this is the start of the authors' own summary.
- Who it was tested in
- Not stated
- Kind of research
- A study
The science
- Original title
- CD8+ T cell transcriptional reprogramming toward TCF7-low cytotoxicity drives immune aging in viral ARDS.
- Authors
- Li K, Ainiwaer K, Song L et al.
- Journal
- iScience
- Published
- Oct 19, 2026
- Study type
- Study
- PMID
- 42894802 ↗
Abstract
Viral acute respiratory distress syndrome (ARDS) exhibits distinct clinical outcomes across age groups, but the immune mechanisms underlying this disparity remain unclear. Here, we integrated single-cell transcriptomic profiling, T cell receptor repertoire analysis, serum proteomics, and functional validation to characterize age-dependent T cell remodeling in influenza-associated ARDS. Adult ARDS was characterized by reduced T cell receptor diversity, expansion of CD8+ effector memory T cells, and enhanced cytotoxic programs marked by increased granzyme B (GZMB) expression compared with pediatric ARDS. At the transcriptional level, adult CD8+ effector memory T cells displayed a TCF7-low state associated with activation of a TGFB1-related RUNX3/PRDM1 program. In vitro experiments further demonstrated that TGFB1 promoted cytotoxic programming in CD8+ effector memory T cells and increased epithelial injury in a co-culture model. These findings identify age-associated CD8+ T cell remodeling as a potential mechanism contributing to immune dysregulation in viral ARDS.
Li K, Ainiwaer K, Song L et al. CD8+ T cell transcriptional reprogramming toward TCF7-low cytotoxicity drives immune aging in viral ARDS. iScience. 2026. doi:10.1016/j.isci.2026.117774. PMID: 42894802. https://pubmed.ncbi.nlm.nih.gov/42894802/