ArticleCellular & molecular immunology2025
Metabolic rewiring controlled by HIF-1α tunes IgA-producing B-cell differentiation and intestinal inflammation.
Article in Cellular & molecular immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- Feeding microbes to feed the Gut: inulin reprograms intestinal epithelial metabolism and proliferation through HIF1α.Gut microbes · 2026Review
- A guide to B cell metabolism.Nature reviews. Immunology · 2026Review
- HnRNPK restrains memory precursor and plasma cell differentiation to control germinal center B-cell output.Cellular & molecular immunology · 2026Article
- Metabolic determinants of autoimmune kidney diseases.Nature reviews. Nephrology · 2026Review
- Oxygen homeostasis: new insight of gut microbiota-host interactions.NPJ biofilms and microbiomes · 2026Review
- The gut-bone-inflammation axis: intestinal barrier disruption as a central driver of osteoporosis.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2026Review
- Hypoxia Independently Induces AID Expression in CH12 B Cells.European journal of immunology · 2026Article
- Dysfunction of mitochondria in intestinal epithelial cells: a key player in the pathogenesis of inflammatory bowel diseases.Gastroenterology report · 2026Review
- Regulatory B Cells in Tumor Microenvironment.Current issues in molecular biology · 2026Review
- Hypoxia-Inducible Factors in Rheumatoid Arthritis: Central Pathogenic Roles and Therapeutic Opportunities.Journal of inflammation research · 2026Review
- Imbalanced IgA-IgG class switching recombination: a novel mechanism of gut immune dysregulation in inflammatory bowel disease.Frontiers in immunology · 2026Review
- CAF-derived BHB modulates FXR1-Kbhb and NK-cell lipid metabolism in osteosarcoma.International journal of biological sciences · 2026Article
- Bee venom acupuncture therapy ameliorates ulcerative colitis by reducing inflammatory response, oxidative stress, and suppressing the NF-κB/HIF-1α pathway.Open life sciences · 2026Article
- Bridging the gaps: the gut-lung axis and microbial metabolites in the pathogenesis and treatment of pulmonary fibrosis.Frontiers in medicine · 2026Review
- Rg1-preconditioned adipose-derived mesenchymal stromal cells alleviate colitis via exosome-mediated Inhibition of macrophage glycolysis through RAS signaling.Stem cell research & therapy · 2025Article
- How lactate and lactylation shape the immunity system in atherosclerosis (Review).International journal of molecular medicine · 2025Review
- Roxadustat as a Hypoxia-Mimetic Agent: Erythropoietic Mechanisms, Bioanalytical Detection, and Regulatory Considerations in Sports Medicine.Current issues in molecular biology · 2025Review
- Redox Regulation and Glucose Metabolism in the Stallion Spermatozoa.Antioxidants (Basel, Switzerland) · 2025Review
- Targeting hypoxia-inducible factor 1α in chronic graft-versus-host disease to enhance graft-versus-leukemia responses: implications for nanotherapeutics.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Germinal centers where B cells undergo clonal expansion and antibody affinity maturation are hypoxic microenvironments. However, the function of hypoxia-inducible factor (HIF)-1α in immunoglobulin production remains incompletely characterized. Here, we demonstrated that B cells lacking HIF-1α exhibited significantly lower glycolytic metabolism and impaired IgA production. Loss of HIF-1α in B cells affects IgA-producing B-cell differentiation and exacerbates dextran sodium sulfate (DSS)-induced colitis. Conversely, promoting HIF-1α stabilization via a PHD inhibitor roxadustat enhances IgA class switching and alleviates intestinal inflammation. Mechanistically, HIF-1α facilitates IgA class switching through acetyl-coenzyme A (acetyl-CoA) accumulation, which is essential for histone H3K27 acetylation at the Sα region. Consequently, supplementation with acetyl-CoA improved defective IgA production in Hif1a-deficient B cells and limited experimental colitis. Collectively, these findings highlight the critical importance of HIF-1α in IgA class switching and the potential for targeting the HIF-1α-dependent metabolic‒epigenetic axis to treat inflammatory bowel diseases and other inflammatory disorders.
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