ArticleThe Journal of biological chemistry2014
An immunogenic peptide in the A-box of HMGB1 protein reverses apoptosis-induced tolerance through RAGE receptor.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
What it found
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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.
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Who cites it
44 citing papers in PubMed, 71 citations in OpenAlex.
- Engineered HMGB1 construct with tandem Box B domains promotes tissue regeneration without potential for inflammation.iScience · 2026Article
- Revealing the Biological Effect of theJournal of the American Chemical Society · 2026Article
- Vagus nerve control of HMGB1 accessibility: a bioelectronic strategy for inflammation and pain.Bioelectronic medicine · 2026Review
- RAGE Signalling in Acute Inflammatory Disorders: Therapeutic Potential of Natural Products.Biomolecules · 2026Review
- Sex-Specific Reversal of Stress-Induced Depressogenic Behaviors by Inhibition of HMGB1, TLR4, and NF-κB Signaling.Molecular neurobiology · 2026Article
- CanPharmaceuticals (Basel, Switzerland) · 2025Review
- Physiological significance of antithrombin D-helix interaction with vascular GAGs.Blood advances · 2025Article
- Role of the Receptor for Advanced Glycation End Products (RAGE) and Its Ligands in Inflammatory Responses.Biomolecules · 2024Review
- The HMGB1-RAGE axis in nucleus accumbens facilitates cocaine-induced conditioned place preference via modulating microglial activation.Brain and behavior · 2024Article
- RAGE Is a Receptor for SARS-CoV-2 N Protein and Mediates N Protein-induced Acute Lung Injury.American journal of respiratory cell and molecular biology · 2023Article
- The role of HMGB1 in COVID-19-induced cytokine storm and its potential therapeutic targets: A review.Immunology · 2023Review
- High Mobility Group Box 1 (HMGB1): Potential Target in Sepsis-Associated Encephalopathy.Cells · 2023Review
- HMGB1 is a critical molecule in the pathogenesis of Gram-negative sepsis.Journal of intensive medicine · 2022Review
- Immunogenic Cell Death, DAMPs and Prothymosin α as a Putative Anticancer Immune Response Biomarker.Cells · 2022Review
- Targeting HMGB1 for the treatment of sepsis and sepsis-induced organ injury.Acta pharmacologica Sinica · 2022Review
- The mechanism of HMGB1 secretion and release.Experimental & molecular medicine · 2022Review
- Post-Translational Modification of HMGB1 Disulfide Bonds in Stimulating and Inhibiting Inflammation.Cells · 2021Review
- PNS protects brain against ischemic injury by acting as an antagonist for AGE/RAGE signaling.Clinical and translational medicine · 2021Article
- High-Mobility Group Box-1 and Its Potential Role in Perioperative Neurocognitive Disorders.Cells · 2021Review
- Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Apoptotic cells trigger immune tolerance in engulfing phagocytes. This poorly understood process is believed to contribute to the severe immunosuppression and increased susceptibility to nosocomial infections observed in critically ill sepsis patients. Extracellular high mobility group box 1 (HMGB1) is an important mediator of both sepsis lethality and the induction of immune tolerance by apoptotic cells. We have found that HMGB1 is sensitive to processing by caspase-1, resulting in the production of a fragment within its N-terminal DNA-binding domain (the A-box) that signals through the receptor for advanced glycation end products (RAGE) to reverse apoptosis-induced tolerance. In a two-hit mouse model of sepsis, we show that tolerance to a secondary infection and its associated mortality were effectively reversed by active immunization with dendritic cells treated with HMGB1 or the A-box fragment, but not a noncleavable form of HMGB1. These findings represent a novel link between caspase-1 and HMGB1, with potential therapeutic implications in infectious and inflammatory diseases.
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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.