ArticleImmunology2003
P27kip1 regulates the cell cycle arrest and survival of activated T lymphocytes in response to interleukin-2 withdrawal.
Article in Immunology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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
7 citing papers in PubMed, 20 citations in OpenAlex.
- Cell cycle arrest enhances CD8Nature immunology · 2026Article
- Low CDKN1B Expression Associated with Reduced CD8+ T Lymphocytes Predicts Poor Outcome in Breast Cancer in a Machine Learning Analysis.Journal of personalized medicine · 2023Article
- Siah2 control of T-regulatory cells limits anti-tumor immunity.Nature communications · 2020Article
- The nuclear mitotic apparatus protein NuMA controls rDNA transcription and mediates the nucleolar stress response in a p53-independent manner.Nucleic acids research · 2017Article
- HelicoVax: epitope-based therapeutic Helicobacter pylori vaccination in a mouse model.Vaccine · 2011Article
- p27Kip1 and p130 cooperate to regulate hematopoietic cell proliferation in vivo.Molecular and cellular biology · 2006Article
- Inducible nitric oxide synthase in T cells regulates T cell death and immune memory.The Journal of clinical investigation · 2004Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The majority of activated T lymphocytes undergo cell death at the end of a primary immune response, while a minority survive as memory cells. The mechanisms that control the decision between these two fates are unknown. In the present study we examined the response of activated T cells to interleukin-2 (IL-2) withdrawal. Within hours, the percentage of T lymphocytes in cell cycle showed a steady decrease, while the percentage arrested in G1 increased proportionally. Deprivation of IL-2 resulted in upregulation of the cell cycle inhibitor p27kip1. Comparison with resting T-cell populations revealed that the highest expression of p27kip1 occurs in activated T cells undergoing cell cycle arrest following IL-2 withdrawal. T cells deficient in p27kip1 expression showed an impaired ability to undergo cell cycle arrest in response to IL-2 deprivation. Moreover, T cells deficient in p27kip1 showed significantly more apoptosis after IL-2 withdrawal. Collectively, this study demonstrates that p27kip1 regulates both the cell cycle arrest and the apoptosis of antigen-specific T lymphocytes.
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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.