ArticleArthritis research & therapy2015
High mobility group box 1 contributes to anti-neutrophil cytoplasmic antibody-induced neutrophils activation through receptor for advanced glycation end products (RAGE) and Toll-like receptor 4.
Article in Arthritis research & therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
20 citing papers in PubMed, 37 citations in OpenAlex.
- Danger-associated molecular pattern molecules and the receptor for advanced glycation end products enhance ANCA-induced responses.Rheumatology (Oxford, England) · 2022Article
- Immunogenic cell death as driver of autoimmunity in granulomatosis with polyangiitis.Frontiers in immunology · 2022Review
- Granulomatous Inflammation in ANCA-Associated Vasculitis.International journal of molecular sciences · 2021Review
- Review
- Immunopathogenesis of ANCA-Associated Vasculitis.International journal of molecular sciences · 2020Review
- Microparticles expressing myeloperoxidase as potential biomarkers in anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitides (AAV).Journal of molecular medicine (Berlin, Germany) · 2020Article
- ANCA-associated vasculitis.Nature reviews. Disease primers · 2020Review
- Association of serum high mobility group box 1 levels with disease activity and renal involvement in patients with systemic vasculitis.Medicine · 2019Observational
- Targeting Complement Pathways in Polytrauma- and Sepsis-Induced Multiple-Organ Dysfunction.Frontiers in immunology · 2019Review
- PRAK Is Required for the Formation of Neutrophil Extracellular Traps.Frontiers in immunology · 2019Article
- Intrarenal Toll-like receptor 4 and Toll-like receptor 2 expression correlates with injury in antineutrophil cytoplasmic antibody-associated vasculitis.American journal of physiology. Renal physiology · 2018Article
- Endotoxemia induces lung-brain coupling and multi-organ injury following cerebral ischemia-reperfusion.Experimental neurology · 2017Article
- HMGB1 contributes to glomerular endothelial cell injury in ANCA-associated vasculitis through enhancing endothelium-neutrophil interactions.Journal of cellular and molecular medicine · 2017Article
- High mobility group box-1 contributes to anti-myeloperoxidase antibody-induced glomerular endothelial cell injury through a moesin-dependent route.Arthritis research & therapy · 2017Article
- Complement in ANCA-associated vasculitis: mechanisms and implications for management.Nature reviews. Nephrology · 2017Review
- Current and novel biomarkers in anti-neutrophil cytoplasm-associated vasculitis.Clinical kidney journal · 2016Article
- Innate immune cells in the pathogenesis of primary systemic vasculitis.Rheumatology international · 2016Review
- High-mobility group box 1 potentiates antineutrophil cytoplasmic antibody-inducing neutrophil extracellular traps formation.Arthritis research & therapy · 2016Article
- Disruption of a Regulatory Network Consisting of Neutrophils and Platelets Fosters Persisting Inflammation in Rheumatic Diseases.Frontiers in immunology · 2016Review
- Contribution of dendritic cells to the autoimmune pathology of systemic lupus erythematosus.Immunology · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionHigh mobility group box-1 (HMGB1), a typical damage-associated molecular pattern (DAMP) protein, is associated with inflammatory conditions and tissue damage. Our recent study found that circulating HMGB1 levels could reflect the disease activity of antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV). The current study aimed to investigate whether HMGB1 participated in ANCA-induced neutrophil activation, which is one of the most important pathogenic aspects in the development of AAV.
methodsThe various effects of HMGB1 in ANCA-induced neutrophil activation were measured. Antagonists for relevant receptors and signaling molecules were employed.
resultsANCA antigens translocation on neutrophils primed with HMGB1 was significantly higher than non-primed neutrophils. The levels of respiratory burst and degranulation increased significantly in HMGB1-primed neutrophils activated with ANCA-positive IgG, as compared with non-primed neutrophils. Furthermore, blocking Toll-like receptor 4 (TLR4) and receptor for advanced glycation end products (RAGE), rather than TLR2, resulted in a significant decrease in HMGB1-induced ANCA antigens translocation, respiratory burst and degranulation. Similar effects were also found when blocking MyD88 and NF-κB.
conclusionsHMGB1 could prime neutrophils by increasing ANCA antigens translocation, and the primed neutrophils could be further induced by ANCA, resulting in the respiratory burst and degranulation. This process is TLR4- and RAGE-dependent through the MyD88/NF-κB pathway.
Indexed as
Identifiers
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.