ArticleJournal of immunology (Baltimore, Md. : 1950)2011
Membrane-associated CD93 regulates leukocyte migration and C1q-hemolytic activity during murine peritonitis.
Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- Diagnostic and Prognostic Role of CD93 in Cardiovascular Disease: A Systematic Review.Biomolecules · 2023Pooled it
- CD93 in Health and Disease: Bridging Physiological Functions and Clinical Applications.International journal of molecular sciences · 2025Review
- Sialyl LewisACS medicinal chemistry letters · 2025Article
- Role of CD93 in Health and Disease.Cells · 2023Review
- CD93 maintains endothelial barrier function by limiting the phosphorylation and turnover of VE-cadherin.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- Soluble CD93 lectin-like domain sequesters HMGB1 to ameliorate inflammatory diseases.Theranostics · 2023Article
- TheJournal of inflammation research · 2023Article
- CD93 is Associated with Glioma-related Malignant Processes and Immunosuppressive Cell Infiltration as an Inspiring Biomarker of Survivance.Journal of molecular neuroscience : MN · 2022Article
- CD93 Correlates With Immune Infiltration and Impacts Patient Immunotherapy Efficacy: A Pan-Cancer Analysis.Frontiers in cell and developmental biology · 2022Article
- Soluble Complement Component 1q Receptor 1 (sCD93) Is Associated with Graft Function in Kidney Transplant Recipients.Biomolecules · 2021Article
- C-type lectin domain group 14 proteins in vascular biology, cancer and inflammation.The FEBS journal · 2019Review
- CD93 regulates central nervous system inflammation in two mouse models of autoimmune encephalomyelitis.Immunology · 2018Article
- Soluble CD93 in Serum as a Marker of Allergic Inflammation.Yonsei medical journal · 2017Article
- Soluble CD93 as a Novel Biomarker in Asthma Exacerbation.Allergy, asthma & immunology research · 2016Article
- CD93 gene polymorphism is associated with disseminated colorectal cancer.International journal of colorectal disease · 2015Article
- CD93 and GIPC expression and localization during central nervous system inflammation.Neural regeneration research · 2014Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
CD93 is emerging as a novel regulator of inflammation; however, its molecular function is unknown. CD93 exists as a membrane-associated glycoprotein on the surface of cells involved in the inflammatory cascade, including endothelial and myeloid cells. A soluble form (sCD93) is detectable in blood and is elevated with inflammation. In this study, we demonstrate heightened susceptibility to thioglycollate-induced peritonitis in CD93(-/-) mice. CD93(-/-) mice showed a 1.6-1.8-fold increase in leukocyte infiltration during thioglycollate-induced peritonitis between 3 and 24 h that returned to wild type levels by 96 h. Impaired vascular integrity in CD93(-/-) mice during peritonitis was demonstrated using fluorescence multiphoton intravital microscopy; however, no differences in cytokine or chemokine levels were detected with Luminex Multiplex or ELISA analysis. C1q-hemolytic activity in CD93(-/-) mice was decreased by 22% at time zero and by 46% 3 h after thioglycollate injection, suggesting a defect in the classical complement pathway. Leukocyte recruitment and C1q-hemolytic activity was restored to wild type levels when CD93 was expressed on either hematopoietic cells or nonhematopoietic cells in bone marrow chimeric mice. However, elevated levels of sCD93 in inflammatory fluid were observed only when CD93 was expressed on nonhematopoietic cells. Because cell-associated CD93 was sufficient to restore a normal inflammatory response, these data suggest that cell-associated CD93, and not sCD93, regulates leukocyte recruitment and complement activation during murine peritonitis.
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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.