ArticleJournal of immunology (Baltimore, Md. : 1950)2011
The liver kinase B1 is a central regulator of T cell development, activation, and metabolism.
Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 159 papers.
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Who cites it
159 citing papers in PubMed, 229 citations in OpenAlex.
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- CD8Science China. Life sciences · 2026Review
- Liver kinase B1 maintains natural killer cell survival by regulating redox homeostasis.Cell death & disease · 2026Article
- Tumor-immune metabolic tug-of-war: from immune escape to targeting metabolic rewiring in cancer therapy.Frontiers in cell and developmental biology · 2026Review
- Cellular metabolism in Th9, Th17, and Treg cell differentiation.International immunology · 2025Review
- Autoimmune disease risk gene ANKRD55 promotes TH17 effector function through metabolic modulation.The Journal of experimental medicine · 2025Article
- STK11 coordinates IL-4 signaling with metabolic reprogramming to control M2 macrophage polarization and antitumor immunity.Science advances · 2025Article
- Metabolic regulation of Th17 and Treg cell balance by the mTOR signaling.Metabolism open · 2025Review
- Metabolic Reprogramming of Anti-cancer T Cells: Targeting AMPK and PPAR to Optimize Cancer Immunotherapy.Indian journal of clinical biochemistry : IJCB · 2025Review
- Complex Interplay Between Metabolism and CD4Cardiovascular drugs and therapy · 2024Review
- Physiologically Achievable Concentration of 2-Deoxy-D-Glucose Stimulates IFN-γ Secretion in Activated T Cells In Vitro.International journal of molecular sciences · 2024Article
- Pro-survival signaling regulates lipophagy essential for multiple myeloma resistance to stress-induced death.Cell reports · 2024Article
- Lkb1 orchestrates γδ T-cell metabolic and functional fitness to control IL-17-mediated autoimmune hepatitis.Cellular & molecular immunology · 2024Article
- Immunometabolism in cancer: basic mechanisms and new targeting strategy.Cell death discovery · 2024Review
- Inhibition of AMPK activation inAntimicrobial agents and chemotherapy · 2024Article
- AMPK Alchemy: Therapeutic Potentials in Allergy, Aging, and Cancer.Biomolecules & therapeutics · 2024Review
- Nutrient inputs and social metabolic control of T cell fate.Cell metabolism · 2024Review
- SIKs Regulate HDAC7 Stabilization and Cytokine Recall in Late-Stage T Cell Effector Differentiation.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Assessing the gene expression of the adenosine 5'-monophosphate-activated protein kinase (AMPK) and its relation with the IL-6 and IL-10 plasma levels in COVID-19 patients.Molecular biology reports · 2023Article
99 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
T cell activation leads to engagement of cellular metabolic pathways necessary to support cell proliferation and function. However, our understanding of the signal transduction pathways that regulate metabolism and their impact on T cell function remains limited. The liver kinase B1 (LKB1) is a serine/threonine kinase that links cellular metabolism with cell growth and proliferation. In this study, we demonstrate that LKB1 is a critical regulator of T cell development, viability, activation, and metabolism. T cell-specific ablation of the gene that encodes LKB1 resulted in blocked thymocyte development and a reduction in peripheral T cells. LKB1-deficient T cells exhibited defects in cell proliferation and viability and altered glycolytic and lipid metabolism. Interestingly, loss of LKB1 promoted increased T cell activation and inflammatory cytokine production by both CD4(+) and CD8(+) T cells. Activation of the AMP-activated protein kinase (AMPK) was decreased in LKB1-deficient T cells. AMPK was found to mediate a subset of LKB1 functions in T lymphocytes, as mice lacking the α1 subunit of AMPK displayed similar defects in T cell activation, metabolism, and inflammatory cytokine production, but normal T cell development and peripheral T cell homeostasis. LKB1- and AMPKα1-deficient T cells each displayed elevated mammalian target of rapamycin complex 1 signaling and IFN-γ production that could be reversed by rapamycin treatment. Our data highlight a central role for LKB1 in T cell activation, viability, and metabolism and suggest that LKB1-AMPK signaling negatively regulates T cell effector function through regulation of mammalian target of rapamycin activity.
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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.