ArticleProceedings of the National Academy of Sciences of the United States of America2012
Tumor suppressor TSC1 is critical for T-cell anergy.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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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
42 citing papers in PubMed, 59 citations in OpenAlex.
- mTORC2 is crucial for regulating the recombinant Mycobacterium tuberculosis CFP-10 protein-induced phagocytosis in macrophages.BMC immunology · 2025Article
- The Kynurenine Pathway and Indole Pathway in Tryptophan Metabolism Influence Tumor Progression.Cancer medicine · 2025Review
- Deciphering T-cell exhaustion in the tumor microenvironment: paving the way for innovative solid tumor therapies.Frontiers in immunology · 2025Review
- mTORC2 contributes to systemic autoimmunity.Immunology · 2023Article
- Absence of TSC1 Accelerates CD8Aging and disease · 2022Article
- Role of TSC1 in physiology and diseases.Molecular and cellular biochemistry · 2021Review
- Regulation of Intrinsic and Bystander T Follicular Helper Cell Differentiation and Autoimmunity by Tsc1.Frontiers in immunology · 2021Article
- Kynurenine pathway, NADExperimental gerontology · 2020Review
- Mammalian Target of Rapamycin Signaling Enhances Ovalbumin-Induced Neutrophilic Airway Inflammation by Promoting Th17 Cell Polarization in Murine Noneosinophilic Asthma Model.Pediatric allergy, immunology, and pulmonology · 2020Article
- Immunometabolic Network Interactions of the Kynurenine Pathway in Cutaneous Malignant Melanoma.Frontiers in oncology · 2020Article
- The Role of TSC1 in the Macrophages AgainstFrontiers in cellular and infection microbiology · 2020Article
- NLRP3 and mTOR Reciprocally Regulate Macrophage Phagolysosome Formation and Acidification AgainstFrontiers in cell and developmental biology · 2020Article
- Efficient CD4Cre-Mediated Conditional KRas Expression in Alveolar Macrophages and Alveolar Epithelial Cells Causes Fatal Hyperproliferative Pneumonitis.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Suboptimal stimulation by weak agonist epitope variants does not drive dysfunction of HIV-1-specific cytotoxic T lymphocyte clones.AIDS (London, England) · 2019Article
- Advances in nanomedicine for cancer starvation therapy.Theranostics · 2019Review
- Targeting the IDO1 pathway in cancer: from bench to bedside.Journal of hematology & oncology · 2018Review
- Discovery of IDO1 Inhibitors: From Bench to Bedside.Cancer research · 2017Review
- The role of metabolic states in development and disease.Current opinion in genetics & development · 2017Review
- Essential Role of mTORC1 in Self-Renewal of Murine Alveolar Macrophages.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- mTOR is critical for intestinal T-cell homeostasis and resistance to Citrobacter rodentium.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
T-cell anergy is a state of T cells that is hyporesponsive to stimulation via the T-cell receptor and costimulatory molecules and is thought to be important for self-tolerance. How T-cell anergy is regulated is still poorly understood. We report here that tuberous sclerosis (TSC)1 is critical for T-cell anergy. Deficiency of TSC1 resulted in enhanced T-cell proliferation and cytokine production in the absence of cluster of differentiation (CD)28-mediated costimulation, accompanied by enhanced T-cell metabolism. Resistance of TSC1-deficient T cells to anergy is correlated with increased signaling through the mammalian target of rapamycin complex (mTORC)1 and can be reverted by treatment of these cells with mTORC1 inhibitor rapamycin. Expression of the inducible costimulator (ICOS) is increased in TSC1-deficient T cells, which can be inhibited by rapamycin. Simultaneous blockade of both CD28 and ICOS costimulation partially restored sensitivity of TSC1-deficient T cells to anergy induction. Together, our data indicate that TSC1 is crucial for T-cell anergy by inhibiting mTORC1 signaling through both ICOS-dependent and -independent mechanisms.
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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.