ReviewNature reviews. Immunology2019
Metabolic gatekeepers to safeguard against autoimmunity and oncogenic B cell transformation.
Review in Nature reviews. Immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
31 citing papers in PubMed, 52 citations in OpenAlex.
- Alternative oncogenic drivers and sensitivity to BTK inhibition in CRISPR/Cas gene-edited human DLBCL cell models.Blood neoplasia · 2026Article
- Therapeutic effects of a synthetic glabridin derivative on metabolic immuno-regulation and salivary gland functional restoration in experimental Sjögren's syndrome.Experimental & molecular medicine · 2026Article
- The Role of the Pentose Phosphate Pathway in Cardiovascular Diseases.Cardiovascular drugs and therapy · 2026Review
- Impaired suppressive effect of FoxP3 regulatory T cells on B cells in multiple sclerosis.Journal of neuroinflammation · 2026Article
- Metabolic reprogramming promotes apoptosis resistance in acute lymphoblastic leukemia through CASP3 lactylation.Molecular cancer · 2025Article
- B cell immunometabolism in health and disease.Nature immunology · 2025Review
- Metabolic regulation of the immune system in health and diseases: mechanisms and interventions.Signal transduction and targeted therapy · 2024Review
- IL-17B alleviates the pathogenesis of systemic lupus erythematosus by inhibiting FASN-mediated differentiation of B cells.JCI insight · 2024Article
- Concepts in B cell acute lymphoblastic leukemia pathogenesis.Journal of leukocyte biology · 2024Review
- Review
- BAFF neutralization impairs the autoantibody-mediated clearance of dead adipocytes and aggravates obesity-induced insulin resistance.Frontiers in immunology · 2024Article
- Mitochondria: the gatekeepers between metabolism and immunity.Frontiers in immunology · 2024Review
- PD-1 instructs a tumor-suppressive metabolic program that restricts glycolysis and restrains AP-1 activity in T cell lymphoma.Nature cancer · 2023Article
- Distinct metabolic requirements regulate B cell activation and germinal center responses.Nature immunology · 2023Article
- IGFBP7 Fuels the Glycolytic Metabolism in B-Cell Precursor Acute Lymphoblastic Leukemia by Sustaining Activation of the IGF1R-Akt-GLUT1 Axis.International journal of molecular sciences · 2023Article
- B cell metabolism in autoimmune diseases: signaling pathways and interventions.Frontiers in immunology · 2023Review
- Enhanced protein synthesis is a defining requirement for neonatal B cell development.Frontiers in immunology · 2023Article
- Article
- Proteomic Profiling of Cryoglobulinemia.Frontiers in immunology · 2022Article
- Deletion of Glut1 in early postnatal cartilage reprograms chondrocytes toward enhanced glutamine oxidation.Bone research · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
B cells face multiple restrictions on glucose and energy metabolism. Their lineage-determining transcription factors repress glucose uptake and pentose phosphate pathway activity, while their low numbers of mitochondria and small cytoplasmic volume set narrow limits for mitochondrial ATP production and autophagy as alternative energy sources. During activation, B cells can balance temporary increases of energy expenditure. However, permanent hyperactivation of kinases, for instance, downstream of an autoreactive B cell receptor (BCR) or a transforming oncogene, can cause energy stress and cell death. Here, I propose that B cell-intrinsic restriction of ATP represents a safeguard to eliminate autoreactive or pre-malignant B cells. If the metabolic gatekeepers are compromised, influx of additional glucose may fuel permanent increases in metabolic demands and pathological B cell proliferation, driven by an autoreactive BCR or a transforming oncogene.
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What OpenQuestion holds
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.