ArticleThe Journal of allergy and clinical immunology2015
Endogenous airway mucins carry glycans that bind Siglec-F and induce eosinophil apoptosis.
Article in The Journal of allergy and clinical immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
57 citing papers in PubMed, 1 synthesis or guideline pooled it, 89 citations in OpenAlex.
- Eosinophils and eosinophil-associated diseases: An update.The Journal of allergy and clinical immunology · 2018Pooled it
- Mucins and Respiratory Virus Infection.Annual review of virology · 2026Review
- Basophils activate splenic B cells and dendritic cells via IL-13 signaling in acute traumatic brain injury.Journal of neuroinflammation · 2025Article
- Siglec-F Deficiency Prevents Fibrosis after Bleomycin-induced Acute Lung Injury.American journal of respiratory cell and molecular biology · 2025Article
- Siglec-F Protects Against Elastase-induced Lung Inflammation and Emphysema in Mice.bioRxiv : the preprint server for biology · 2025Article
- Mucins and Their Roles in Asthma.Immunological reviews · 2025Review
- Breaking Down the Bottlebrush: Atomically Detailed Structural Dynamics of Mucins.Journal of chemical information and modeling · 2024Article
- Emerging cell and molecular targets for treating mucus hypersecretion in asthma.Allergology international : official journal of the Japanese Society of Allergology · 2024Review
- The Exploitation of the Glycosylation Pattern in Asthma: How We Alter Ancestral Pathways to Develop New Treatments.Biomolecules · 2024Review
- GlcNAc6ST2/CHST4 Is Essential for the Synthesis of R-10G-Reactive Keratan Sulfate/SulfatedMolecules (Basel, Switzerland) · 2024Article
- Eosinophil-Epithelial Cell Interactions in Asthma.International archives of allergy and immunology · 2024Review
- MUC5AC Genetic Variation Is Associated With Tuberculous Meningitis Cerebral Spinal Fluid Cytokine Responses and Mortality.The Journal of infectious diseases · 2023Article
- The adaptive microbiome hypothesis and immune interactions in amphibian mucus.Developmental and comparative immunology · 2023Review
- Siglecs in allergy and asthma.Molecular aspects of medicine · 2023Review
- Human sialoglycan ligands for immune inhibitory Siglecs.Molecular aspects of medicine · 2023Review
- Complementary Role of GlcNAc6ST2 and GlcNAc6ST3 in Synthesis of CL40-Reactive Sialylated and Sulfated Glycans in the Mouse Pleural Mesothelium.Molecules (Basel, Switzerland) · 2022Article
- Review
- Siglec-F Promotes IL-33-Induced Cytokine Release from Bone Marrow-Derived Eosinophils Independently of the ITIM and ITIM-like Motif Phosphorylation.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Epigenetic reprogramming of airway macrophages promotes polarization and inflammation in muco-obstructive lung disease.Nature communications · 2021Article
- Mucus composition abnormalities in sinonasal mucosa of chronic rhinosinusitis with and without nasal polyps.Inflammation · 2021Article
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
Abstract
backgroundSialic acid-binding, immunoglobulin-like lectin (Siglec) F is a glycan-binding protein selectively expressed on mouse eosinophils. Its engagement induces apoptosis, suggesting a pathway for ameliorating eosinophilia in the setting of asthma and other eosinophil-associated diseases. Siglec-F recognizes sialylated sulfated glycans in glycan-binding assays, but the identities of endogenous sialoside ligands and their glycoprotein carriers in vivo are unknown.
objectivesTo use mouse lung-derived materials to isolate, biochemically identify, and biologically characterize naturally occurring endogenous glycan ligands for Siglec-F.
methodsLungs from normal and mucin-deficient mice, as well as mouse tracheal epithelial cells, were investigated in vitro and in vivo for the expression of Siglec-F ligands. Western blotting and cytochemistry used Siglec-F-Fc as a probe for directed purification, followed by liquid chromatography-tandem mass spectrometry of recognized glycoproteins. Purified components were tested in mouse eosinophil-binding assays and flow cytometry-based cell death assays.
resultsWe detected mouse lung glycoproteins that bound to Siglec-F; binding was sialic acid dependent. Proteomic analysis of Siglec-F binding material identified Muc5b and Muc4. Cross-affinity enrichment and histochemical analysis of lungs from mucin-deficient mice assigned and validated the identity of Muc5b as one glycoprotein ligand for Siglec-F. Purified mucin preparations carried sialylated and sulfated glycans, bound to eosinophils and induced their death in vitro. Mice conditionally deficient in Muc5b displayed exaggerated eosinophilic inflammation in response to intratracheal installation of IL-13.
conclusionsThese data identify a previously unrecognized endogenous anti-inflammatory property of airway mucins by which their glycans can control lung eosinophilia through engagement of Siglec-F.
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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.