ArticleBlood2011
Cleavage of the CD11b extracellular domain by the leukocyte serprocidins is critical for neutrophil detachment during chemotaxis.
Article in Blood, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 67 citations in OpenAlex.
- Changes in Soluble CD18 in Murine Autoimmune Arthritis and Rheumatoid Arthritis Reflect Disease Establishment and Treatment Response.PloS one · 2016Trial
- Proteomic Portrait of Degranulation Program in Human Circulating Neutrophils Upon Multi-Inflammatory and Infectious Activation.Molecular & cellular proteomics : MCP · 2026Article
- Neutrophil CD11b is a pivotal PANoptosis marker correlated with disease activity in antineutrophil cytoplasmic antibody-associated vasculitis.Apoptosis : an international journal on programmed cell death · 2025Article
- The trapping of live neutrophils by macrophages during infection.Cell death & disease · 2025Article
- Large soluble CD18 complexes with exclusive ICAM-1-binding properties are shed during immune cell migration in inflammation.Journal of translational autoimmunity · 2025Article
- A pan-family screen of nuclear receptors in immunocytes reveals ligand-dependent inflammasome control.Immunity · 2024Article
- NLRP3 exacerbates EAE severity through ROS-dependent NET formation in the mouse brain.Cell communication and signaling : CCS · 2024Article
- ECRG4 mediates host response to cutaneous infection by regulating neutrophil recruitment and adhesion receptor expression.PloS one · 2024Article
- Bioinformatics analysis and identification of hub genes of neutrophils in Kawasaki disease: a pivotal study.Clinical rheumatology · 2023Article
- Targeting Neutrophil βBiomolecules · 2023Review
- Soluble ITGaM and ITGb2 Integrin Subunits Are Involved in Long-Term Pulmonary Complications after COVID-19 Infection.Journal of clinical medicine · 2023Article
- Intravascular Crawling of Patrolling Monocytes: A Lèvy-Like Motility for Unique Search Functions?Frontiers in immunology · 2021Review
- The Promiscuous Profile of Complement Receptor 3 in Ligand Binding, Immune Modulation, and Pathophysiology.Frontiers in immunology · 2021Review
- Integrated analysis identifies AQP9 correlates with immune infiltration and acts as a prognosticator in multiple cancers.Scientific reports · 2020Article
- Neutrophil Modulation in Alpha-1 Antitrypsin Deficiency.Chronic obstructive pulmonary diseases (Miami, Fla.) · 2020Review
- Therapeutic targeting of neutrophil exocytosis.Journal of leukocyte biology · 2020Review
- Current Understanding of Leukocyte Phenotypic and Functional Modulation During Extracorporeal Membrane Oxygenation: A Narrative Review.Frontiers in immunology · 2020Review
- CD11b Signaling Prevents Chondrocyte Mineralization and Attenuates the Severity of Osteoarthritis.Frontiers in cell and developmental biology · 2020Article
- The role of neutrophil granule proteins in neuroinflammation and Alzheimer's disease.Journal of neuroinflammation · 2018Review
- MT4-MMP deficiency increases patrolling monocyte recruitment to early lesions and accelerates atherosclerosis.Nature communications · 2018Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
The β(2)-integrin CD11b/CD18 mediates the firm adhesion of neutrophils (PMNs) to epithelial monolayers, a key step in PMN transepithelial migration. To complete the transmigration process, adherent PMNs must detach from epithelial monolayer surfaces to move forward. The mechanism that governs the detachment of adherent PMNs, however, is not clear. Here, we present evidence that cleavage of the CD11b extracellular domain containing the ligand-binding I-domain by 3 structural and functional related serine proteases (elastase, proteinase-3 and cathepsin G) serves as a novel mechanism for PMN detachment after the initial cell adhesion. Kinetic studies showed that the cleavage of CD11b is positively correlated with PMN detachment and subsequent transmigration. Moreover, the results demonstrated that elastase, proteinase-3 and cathepsin G all cleaved the purified, functionally active form of CD11b in a pattern similar to the CD11b shedding that occurs during PMN transmigration. Their cleavage sites on purified CD11b were located at (761)Thr-Ala(762) (elastase/proteinase-3) and (760)Phe-Thr(761) (cathepsin G), respectively. CD11b cleavage and PMN detachment and chemotaxis, were impaired in elastase/cathepsin G-deficient Beige mice; this defect could be restored by the addition of extracellular elastase. By illustrating CD11b shedding by elastase, proteinase-3 and cathepsin G as a novel mechanism for PMN detachment, our study provides novel therapeutic targets for controlling inflammation.
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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.