ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2021
The energy sensor AMPK orchestrates metabolic and translational adaptation in expanding T helper cells.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 15 citations in OpenAlex.
- Emerging Roles for Metabolism in Myocardial Inflammation During Heart Failure.Immunological reviews · 2026Review
- TEAD4 Promotes Myogenic Differentiation of Porcine Skeletal Muscle Satellite Cells.Animals : an open access journal from MDPI · 2026Article
- Dysregulated immunometabolism in gut inflammation.Acta biochimica et biophysica Sinica · 2026Review
- M2 macrophages and tumor cells engage in a metabolic feedback loop to drive HCC progression.Scientific reports · 2025Article
- Metabolic Reprogramming of Anti-cancer T Cells: Targeting AMPK and PPAR to Optimize Cancer Immunotherapy.Indian journal of clinical biochemistry : IJCB · 2025Review
- Metabolic reprogramming as a therapeutic target for modulating the Th17/Treg balance in autoimmune diseases: a comprehensive review.Frontiers in immunology · 2025Review
- AMPK in Intestinal Health and Disease: A Multifaceted Therapeutic Target for Metabolic and Inflammatory Disorders.Drug design, development and therapy · 2025Review
- T-Cell Metabolic Reprogramming in Atherosclerosis.Biomedicines · 2024Review
- AMPK drives both glycolytic and oxidative metabolism in murine and human T cells during graft-versus-host disease.Blood advances · 2024Article
- Overexpression of AMPKγ2 increases AMPK signaling to augment human T cell metabolism and function.The Journal of biological chemistry · 2024Article
- PRKAG2.2 is essential for FoxA1Science advances · 2023Article
- Article
- AMPK suppresses Th2 cell responses by repressing mTORC2.Experimental & molecular medicine · 2022Article
- MicroRNA-mediated metabolic reprogramming of chimeric antigen receptor T cells.Immunology and cell biology · 2022Article
- The energy sensor AMPK orchestrates metabolic and translational adaptation in expanding T helper cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- The Alterations in and the Role of the Th17/Treg Balance in Metabolic Diseases.Frontiers in immunology · 2021Review
Corrections and comments
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Authors and funding
19 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The importance of cellular metabolic adaptation in inducing robust T cell responses is well established. However, the mechanism by which T cells link information regarding nutrient supply to clonal expansion and effector function is still enigmatic. Herein, we report that the metabolic sensor adenosine monophosphate-activated protein kinase (AMPK) is a critical link between cellular energy demand and translational activity and, thus, orchestrates optimal expansion of T cells in vivo. AMPK deficiency did not affect T cell fate decision, activation, or T effector cell generation; however, the magnitude of T cell responses in murine in vivo models of T cell activation was markedly reduced. This impairment was global, as all T helper cell subsets were similarly sensitive to loss of AMPK which resulted in reduced T cell accumulation in peripheral organs and reduced disease severity in pathophysiologically as diverse models as T cell transfer colitis and allergic airway inflammation. T cell receptor repertoire analysis confirmed similar clonotype frequencies in different lymphoid organs, thereby supporting the concept of a quantitative impairment in clonal expansion rather than a skewed qualitative immune response. In line with these findings, in-depth metabolic analysis revealed a decrease in T cell oxidative metabolism, and gene set enrichment analysis indicated a major reduction in ribosomal biogenesis and mRNA translation in AMPK-deficient T cells. We, thus, provide evidence that through its interference with these delicate processes, AMPK orchestrates the quantitative, but not the qualitative, manifestation of primary T cell responses in vivo.
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