ArticleJournal of leukocyte biology2015
Regulation of CXCR2 expression and function by a disintegrin and metalloprotease-17 (ADAM17).
Article in Journal of leukocyte biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 38 citations in OpenAlex.
- Trial
- Endothelial ADAM17 facilitates neutrophil migration and pulmonary microvascular permeability in acute lung inflammation.Journal of biomedical science · 2026Article
- DVT-primed neutrophils reshape the brain microenvironment to promote brain metastasis.bioRxiv : the preprint server for biology · 2026Article
- Distinctive Macrophage Migration Inhibitory Factor Receptor Patterns and Soluble Biomarkers in Rheumatoid Arthritis: Unveiling Key Associations with Disease Activity.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2025Article
- Inhibition of ADAM17 attenuates high glucose-induced angiogenesis and inflammation in endothelial cells partly through down-regulation of GRO-α/CXCR2 expression: implications in peritoneal dialysis.Clinical and experimental nephrology · 2024Article
- CXCL17 is a proinflammatory chemokine and promotes neutrophil trafficking.Journal of leukocyte biology · 2024Article
- Chemokine Cxcl1-Cxcl2 heterodimer is a potent neutrophil chemoattractant.Journal of leukocyte biology · 2023Article
- Review
- A Novel Selective Inhibitor JBI-589 Targets PAD4-Mediated Neutrophil Migration to Suppress Tumor Progression.Cancer research · 2022Article
- Short-Term Effect of SARS-CoV-2 Spike Protein Receptor-Binding Domain-Specific Antibody Induction on Neutrophil-Mediated Immune Response in Mice.International journal of molecular sciences · 2022Article
- Beyond Hemostasis: Platelet Innate Immune Interactions and Thromboinflammation.International journal of molecular sciences · 2022Review
- Soluble forms of cytokine and growth factor receptors: mechanisms of generation and modes of action in the regulation of local and systemic inflammation.FEBS letters · 2022Review
- Neutrophils self-limit swarming to contain bacterial growth in vivo.Science (New York, N.Y.) · 2021Article
- Ectodomain shedding by ADAM17 (a disintegrin and metalloproteinase 17) in canine neutrophils.Veterinary immunology and immunopathology · 2021Article
- Leptin Receptor q223r Polymorphism InfluencesFrontiers in cellular and infection microbiology · 2021Article
- ADAM17, A Key Player of Cardiac Inflammation and Fibrosis in Heart Failure Development During Chronic Catecholamine Stress.Frontiers in cell and developmental biology · 2021Review
- Blocking ADAM17 Function with a Monoclonal Antibody Improves Sepsis Survival in a Murine Model of Polymicrobial Sepsis.International journal of molecular sciences · 2020Article
- Review
- Article
- Neutrophils Induce a Novel Chemokine Receptors Repertoire During Influenza Pneumonia.Frontiers in cellular and infection microbiology · 2019Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The chemokine receptor CXCR2 is expressed at high levels on circulating neutrophils and is critical for directing their migration to sites of inflammation. CXCR2 surface levels are rapidly modulated by 2 mechanisms-cell internalization and recycling upon ligand binding-and by a metalloprotease activity following overt neutrophil activation by nonligand stimuli. The latter process has only been described in human neutrophils, and essentially, nothing is known about its functional relevance and the specific protease involved. We show that targeting ADAM17 in mouse and human neutrophils blocks CXCR2 down-regulation induced by nonligand stimuli but not by chemokine ligands. This was determined by use of a selective ADAM17 inhibitor, an ADAM17 function-blocking antibody, and ADAM17 gene-targeted mice. CXCR2 is known to undergo a marked down-regulation during various inflammatory disorders, and this is associated with impaired neutrophil recruitment. We show that blocking ADAM17 activity reduced CXCR2 down-regulation on circulating neutrophils and enhanced their recruitment during acute inflammation, which was reversed by a CXCR2 inhibitor. Taken together, our findings demonstrate that unlike CXCR2 internalization, ADAM17 induction down-regulates the receptor in an irreversible manner and may serve as a master switch in controlling CXCR2 function, but may also contribute to neutrophil dysfunction during excessive inflammation.
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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.