ArticleEMBO reports2023
Excessive apoptosis of Rip1-deficient T cells leads to premature aging.
Article in EMBO reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- Ripk1 is critical for preserving effector regulatory T cells and the suppressive transcriptional program in regulatory T cells.Cell death and differentiation · 2026Article
- Article
- Aging reshapes the adaptive immune system from healer to saboteur.Nature aging · 2025Review
- CD4 T cell therapy counteracts inflammaging and senescence by preserving gut barrier integrity.Science immunology · 2025Article
- Targeting T-cell Aging to Remodel the Aging Immune System and Revitalize Geriatric Immunotherapy.Aging and disease · 2025Review
- Article
- The network structural entropy for single-cell RNA sequencing data during skin aging.Briefings in bioinformatics · 2024Article
- RIPK1 protects naive and regulatory T cells from TNFR1-induced apoptosis.Cell death and differentiation · 2024Article
- Not to be and how not to be: the questions of Tregs controlled by RIPK1.Cellular & molecular immunology · 2024Article
- Excessive apoptosis of Rip1-deficient T cells leads to premature aging.EMBO reports · 2023Article
Corrections and comments
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Authors and funding
27 authors at 3 institutions in 1 country.
Funding
Abstract
In mammals, the most remarkable T cell variations with aging are the shrinking of the naïve T cell pool and the enlargement of the memory T cell pool, which are partially caused by thymic involution. However, the mechanism underlying the relationship between T-cell changes and aging remains unclear. In this study, we find that T-cell-specific Rip1 KO mice show similar age-related T cell changes and exhibit signs of accelerated aging-like phenotypes, including inflammation, multiple age-related diseases, and a shorter lifespan. Mechanistically, Rip1-deficient T cells undergo excessive apoptosis and promote chronic inflammation. Consistent with this, blocking apoptosis by co-deletion of Fadd in Rip1-deficient T cells significantly rescues lymphopenia, the imbalance between naïve and memory T cells, and aging-like phenotypes, and prolongs life span in T-cell-specific Rip1 KO mice. These results suggest that the reduction and hyperactivation of T cells can have a significant impact on organismal health and lifespan, underscoring the importance of maintaining T cell homeostasis for healthy aging and prevention or treatment of age-related diseases.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.