ArticleAutophagy2015
Autophagy regulates T lymphocyte proliferation through selective degradation of the cell-cycle inhibitor CDKN1B/p27Kip1.
Article in Autophagy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 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.
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Who cites it
68 citing papers in PubMed, 101 citations in OpenAlex.
- The Sleeping Giant: Metabolism and Autophagy in the Generation and Survival of Dormant Polyploid Giant Cancer Cells.MedComm · 2026Review
- Maternal Obesity Reprograms Differentiation Trajectories of Fetal Hematopoietic Stem and Progenitor Cells Through Altered Inflammatory Signaling.bioRxiv : the preprint server for biology · 2026Article
- Autophagy modulation in gynaecologic oncology: insights into immune regulation and therapeutic potential.Frontiers in immunology · 2026Review
- Autophagy-regulated mitochondrial inheritance controls early CD8Nature cell biology · 2026Article
- Mechanism and role of regulated cell death in tumor immunity and immunotherapy.Cancer communications (London, England) · 2025Review
- Role of autophagy in rejection after solid organ transplantation: A systematic review of the literature.World journal of transplantation · 2025Review
- Autophagy in tumor immune escape and immunotherapy.Molecular cancer · 2025Review
- Autophagy repression by antigen and cytokines shapes mitochondrial, migration and effector machinery in CD8 T cells.Nature immunology · 2025Article
- Genomic Regions Associated with Resistance to Gastrointestinal Nematode Parasites in Sheep-A Review.Genes · 2024Review
- The 330 risk loci known for systemic lupus erythematosus (SLE): a review.Frontiers in lupus · 2024Article
- Targeted Mevalonate Pathway and Autophagy in Antitumor Immunotherapy.Current cancer drug targets · 2024Review
- Exploiting autophagy balance in T and NK cells as a new strategy to implement adoptive cell therapies.Molecular cancer · 2023Review
- Metabolic reprogramming, autophagy, and ferroptosis: Novel arsenals to overcome immunotherapy resistance in gastrointestinal cancer.Cancer medicine · 2023Review
- Proteostasis in T cell aging.Seminars in immunology · 2023Review
- Streptococcal Arginine Deiminase Inhibits T Lymphocyte Differentiation In Vitro.Microorganisms · 2023Article
- Ferroptosis, autophagy, tumor and immunity.Heliyon · 2023Review
- Immunomodulatory effects of umbilical mesenchymal stem cell-derived exosomes on CD4Inflammopharmacology · 2023Article
- Harnessing Autophagy to Overcome Antigen-Specific T-Cell Dysfunction: Implication for People Living with HIV-1.International journal of molecular sciences · 2023Review
- Crosstalk between autophagy and metabolic regulation of (CAR) T cells: therapeutic implications.Frontiers in immunology · 2023Review
- Crosstalk between autophagy and immune cell infiltration in the tumor microenvironment.Frontiers in medicine · 2023Review
8 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The highly conserved cellular degradation pathway, macroautophagy, regulates the homeostasis of organelles and promotes the survival of T lymphocytes. Previous results indicate that Atg3-, Atg5-, or Pik3c3/Vps34-deficient T cells cannot proliferate efficiently. Here we demonstrate that the proliferation of Atg7-deficient T cells is defective. By using an adoptive transfer and Listeria monocytogenes (LM) mouse infection model, we found that the primary immune response against LM is intrinsically impaired in autophagy-deficient CD8(+) T cells because the cell population cannot expand after infection. Autophagy-deficient T cells fail to enter into S-phase after TCR stimulation. The major negative regulator of the cell cycle in T lymphocytes, CDKN1B, is accumulated in autophagy-deficient naïve T cells and CDKN1B cannot be degraded after TCR stimulation. Furthermore, our results indicate that genetic deletion of one allele of CDKN1B in autophagy-deficient T cells restores proliferative capability and the cells can enter into S-phase after TCR stimulation. Finally, we found that natural CDKN1B forms polymers and is physiologically associated with the autophagy receptor protein SQSTM1/p62 (sequestosome 1). Collectively, autophagy is required for maintaining the expression level of CDKN1B in naïve T cells and selectively degrades CDKN1B after TCR stimulation.
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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.