ArticleJournal of the American Society of Nephrology : JASN2008
Mechanisms of ANCA-mediated leukocyte-endothelial cell interactions in vivo.
Article in Journal of the American Society of Nephrology : JASN, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 85 citations in OpenAlex.
- Functional classification of antineutrophil cytoplasmic antibody (ANCA) and its relation with clinical parameters of ANCA-associated vasculitis.Biochemistry and biophysics reports · 2026Article
- Potential of serum sulfatide levels as a marker for classification and disease activity in lupus nephritis.Frontiers in immunology · 2025Article
- The involvement of NETs in ANCA-associated vasculitis.Frontiers in immunology · 2023Review
- A historical review of experimental imaging of the beating heart coronary microcirculation in vivo.Journal of anatomy · 2023Review
- Recipient myeloperoxidase-producing cells regulate antibody-mediated acute versus chronic kidney allograft rejection.JCI insight · 2021Article
- Identification of neutrophil β2-integrin LFA-1 as a potential mechanistic biomarker in ANCA-associated vasculitis via microarray and validation analyses.Arthritis research & therapy · 2021Article
- ANCA-associated vasculitis.Nature reviews. Disease primers · 2020Review
- Animal Models of ANCA Associated Vasculitis.Frontiers in immunology · 2020Review
- Antineutrophil cytoplasmic antibodies (ANCA) - their role in pathogenesis, diagnosis, and treatment monitoring of ANCA-associated vasculitis.Central-European journal of immunology · 2020Review
- Pathogenesis of ANCA-Associated Pulmonary Vasculitis.Seminars in respiratory and critical care medicine · 2018Review
- Complement Factor H Inhibits Anti-Neutrophil Cytoplasmic Autoantibody-Induced Neutrophil Activation by Interacting With Neutrophils.Frontiers in immunology · 2018Article
- Immunomodulation with eicosapentaenoic acid supports the treatment of autoimmune small-vessel vasculitis.Scientific reports · 2014Article
- Syndecan-3 is selectively pro-inflammatory in the joint and contributes to antigen-induced arthritis in mice.Arthritis research & therapy · 2014Article
- Proposal of anti-moesin as a novel biomarker for ANCA-associated vasculitis.Clinical and experimental nephrology · 2013Review
- Genetically determined severity of anti-myeloperoxidase glomerulonephritis.The American journal of pathology · 2013Article
- The immunodominant myeloperoxidase T-cell epitope induces local cell-mediated injury in antimyeloperoxidase glomerulonephritis.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Aminobenzoic acid hydrazide, a myeloperoxidase inhibitor, alters the adhesive properties of neutrophils isolated from acute myocardial infarction patients.Heart and vessels · 2012Article
- Endothelium-neutrophil interactions in ANCA-associated diseases.Journal of the American Society of Nephrology : JASN · 2012Review
- Pathogenesis of anti-neutrophil cytoplasmic autoantibody (ANCA)-associated vasculitis.Clinical and experimental immunology · 2011Review
- Immunoglobulin subclass determines ability of immunoglobulin (Ig)G to capture and activate neutrophils presented as normal human IgG or disease-associated anti-neutrophil cytoplasm antibody (ANCA)-IgG.Clinical and experimental immunology · 2011Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
Abstract
Anti-myeloperoxidase (anti-MPO) antibodies have been implicated in the pathogenesis of small-vessel vasculitis, but the molecular mechanisms by which these antibodies contribute to disease are unknown. For determination of how anti-MPO antibodies affect inflammatory cell recruitment in small-vessel vasculitis, intravital microscopy was used to monitor leukocyte behavior in the accessible cremasteric microvessels under various experimental conditions. After local pretreatment of the cremaster muscle with cytokines (TNF-alpha, IL-1beta, or keratinocyte-derived chemokine), administration of anti-MPO IgG to wild-type mice reduced leukocyte rolling in favor of augmented adhesion to and transmigration across the endothelium. This led to a decrease in the number of systemic circulating leukocytes and, similar to the early events in the development of vasculitic lesions, an increase in leukocyte recruitment to renal and pulmonary tissue. TNF-alpha led to the greatest recruitment of inflammatory cells, and IL-1beta led to the least. When anti-CD18 was co-administered, anti-MPO IgG did not affect leukocyte rolling, adhesion, or transmigration; similarly, anti-MPO IgG did not produce these effects in Fc receptor gamma chain-/- mice. This study provides direct in vivo evidence of enhanced leukocyte-endothelial cell interactions in the presence of anti-MPO IgG and highlights the critical roles of Fcgamma receptors and beta2 integrins in mediating these interactions. In addition, it suggests that neutrophils primed by cytokines in the presence of anti-MPO IgG can have systemic effects and target specific vascular beds.
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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.