ArticleThe Journal of biological chemistry2011
Complement receptor Mac-1 is an adaptor for NB1 (CD177)-mediated PR3-ANCA neutrophil activation.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 109 citations in OpenAlex.
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- Neutrophils and Platelets as Key Players in the Pathogenesis of ANCA-Associated Vasculitis and Potential Sources of Disease Activity Biomarkers.Diagnostics (Basel, Switzerland) · 2025Review
- Targeting mitochondrial complex I of CD177Cell reports. Medicine · 2025Article
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- Investigating neutrophil responses to stimuli: Comparative analysis of reactive species-dependent and independent mechanisms.Redox biology · 2025Article
- Molecular analysis of acute pyelonephritis-excessive innate and attenuated adaptive immunity.Life science alliance · 2025Article
- Unveiling CD177: a key player in tumors, autoimmune diseases, and inflammatory disorders.Frontiers in immunology · 2025Review
- Exploring novel protein biomarkers for early-stage diagnosis and prognosis of T-acute lymphoblastic leukemia (T-ALL).Hematology, transfusion and cell therapy · 2024Article
- Dual role of CD177 + neutrophils in inflammatory bowel disease: a review.Journal of translational medicine · 2024Review
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- Construction of a panoramic mRNA map of adult noncystic fibrosis bronchiectasis and a preliminary study of the underlying molecular mechanisms.European journal of medical research · 2024Article
- Sepsis in elderly patients: the role of neutrophils in pathophysiology and therapy.Internal and emergency medicine · 2024Review
- Prognostic value of tumor‑associated CD177Oncology letters · 2024Article
- CD177 is a novel IgG Fc receptor and CD177 genetic variants affect IgG-mediated function.Frontiers in immunology · 2024Article
- Whole blood transcriptomics reveals the enrichment of neutrophil activation pathways during erythema nodosum leprosum reaction.Frontiers in immunology · 2024Article
- Gene network landscape of mouse splenocytes reveals integrin complex as the A151 ODN-responsive hub molecule in the immune transcriptome.Molecular therapy. Nucleic acids · 2023Article
- Using a Network-Based Analysis Approach to Investigate the Involvement ofInternational journal of molecular sciences · 2023Article
- GPR97 triggers inflammatory processes in human neutrophils via a macromolecular complex upstream of PAR2 activation.Nature communications · 2022Article
- Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The glycosylphosphatidylinositol (GPI)-anchored neutrophil-specific receptor NB1 (CD177) presents the autoantigen proteinase 3 (PR3) on the membrane of a neutrophil subset. PR3-ANCA-activated neutrophils participate in small-vessel vasculitis. Since NB1 lacks an intracellular domain, we characterized components of the NB1 signaling complex that are pivotal for neutrophil activation. PR3-ANCA resulted in degranulation and superoxide production in the mNB1(pos)/PR3(high) neutrophils, but not in the mNB1(neg)/PR3(low) subset, whereas MPO-ANCA and fMLP caused similar responses. The NB1 signaling complex that was precipitated from plasma membranes contained the transmembrane receptor Mac-1 (CD11b/CD18) as shown by MS/MS analysis and immunoblotting. NB1 co-precipitation was less for CD11a and not detectable for CD11c. NB1 showed direct protein-protein interactions with both CD11b and CD11a by surface plasmon resonance analysis (SPR). However, when these integrins were presented as heterodimeric transmembrane proteins on transfected cells, only CD11b/CD18 (Mac-1)-transfected cells adhered to immobilized NB1 protein. This adhesion was inhibited by mAb against NB1, CD11b, and CD18. NB1, PR3, and Mac-1 were located within lipid rafts. In addition, confocal microscopy showed the strongest NB1 co-localization with CD11b and CD18 on the neutrophil. Stimulation with NB1-activating mAb triggered degranulation and superoxide production in mNB1(pos)/mPR3(high) neutrophils, and this effect was reduced using blocking antibodies to CD11b. CD11b blockade also inhibited PR3-ANCA-induced neutrophil activation, even when β2-integrin ligand-dependent signals were omitted. We establish the pivotal role of the NB1-Mac-1 receptor interaction for PR3-ANCA-mediated neutrophil activation.
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