ArticleBlood2013
Siglec-E is a negative regulator of acute pulmonary neutrophil inflammation and suppresses CD11b β2-integrin-dependent signaling.
Article in Blood, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 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.
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Who cites it
73 citing papers in PubMed, 108 citations in OpenAlex.
- Loss of erythrocyte sialic acid in sepsis disrupts inhibitory Siglec interactions, driving neutrophil hyperactivation and NET outspread.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Targeting Siglec-E Modulates Macrophage Polarization to Attenuate Cardiac Remodeling After Myocardial Infarction.Journal of cardiovascular translational research · 2026Article
- Innovative approaches targeting innate immune cells to promote organ transplant tolerance.Frontiers in transplantation · 2026Review
- The inhibitory receptor Siglec-E controls antigen-presenting cell activation and T cell-mediated transplant rejection.Science translational medicine · 2025Article
- Mucins and Their Roles in Asthma.Immunological reviews · 2025Review
- The role of mTOR activation in steroid-resistant asthma: insights from particulate matter-induced mouse model and patient studies.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- Siglec-E augments adipose tissue inflammation by modulating TRAF3 signaling and monocytic myeloid-derived suppressor cells during obesity.Frontiers in immunology · 2025Article
- Multi-targeted olink proteomics analyses of cerebrospinal fluid from patients with aneurysmal subarachnoid hemorrhage.Proteome science · 2024Article
- Sialic Acid-Siglec-E Interactions Regulate the Response of Neonatal Macrophages to Group B Streptococcus.ImmunoHorizons · 2024Article
- From mechanism to therapy: the journey of CD24 in cancer.Frontiers in immunology · 2024Review
- Siglec-9 is an inhibitory receptor on human mast cells in vitro.The Journal of allergy and clinical immunology · 2023Article
- Sialic Acids on Tumor Cells Modulate IgA Therapy by Neutrophils via Inhibitory Receptors Siglec-7 and Siglec-9.Cancers · 2023Article
- Structural insights into Siglec-15 reveal glycosylation dependency for its interaction with T cells through integrin CD11b.Nature communications · 2023Article
- Targeting Neutrophil βBiomolecules · 2023Review
- The Interplay between Integrins and Immune Cells as a Regulator in Cancer Immunology.International journal of molecular sciences · 2023Review
- Detailed characterisation of invasive aspergillosis in a murine model of X-linked chronic granulomatous disease shows new insights in infections caused byFrontiers in cellular and infection microbiology · 2023Article
- Hallmarks of the relationship between host andFrontiers in cellular and infection microbiology · 2023Review
- Interactions between Siglec-8 and endogenous sialylated cis ligands restrain cell death induction in human eosinophils and mast cells.Frontiers in immunology · 2023Article
- Myeloid checkpoints for cancer immunotherapy.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2022Article
- CD24-Siglec axis is an innate immune checkpoint against metaflammation and metabolic disorder.Cell metabolism · 2022Article
13 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Neutrophil entry into the lung tissues is a key step in host defense to bacterial and yeast infections, but if uncontrolled can lead to severe tissue damage. Here, we demonstrate for the first time that sialic acid binding Ig-like lectin E (siglec-E) functions to selectively regulate early neutrophil recruitment into the lung. In a model of acute lung inflammation induced by aerosolized lipopolysaccharide, siglec-E-deficient mice exhibited exaggerated neutrophil recruitment that was reversed by blockade of the β2 integrin, CD11b. Siglec-E suppressed CD11b "outside-in" signaling, because siglec-E-deficient neutrophils plated on the CD11b ligand fibrinogen showed exaggerated phosphorylation of Syk and p38 mitogen-activated protein kinase. Sialidase treatment of fibrinogen reversed the suppressive effect of siglec-E on CD11b signaling, suggesting that sialic acid recognition by siglec-E is required for its inhibitory function. Siglec-E in neutrophils was constitutively associated with the tyrosine phosphatase SHP-1 and may therefore function to constitutively dampen inflammatory responses of neutrophils. These data reveal that siglec-E is an important negative regulator of neutrophil recruitment to the lung and β2 integrin-dependent signaling. Our findings have implications for the human functional ortholog, siglec-9, and its potential role in regulating inflammatory lung disease.
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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.