ArticleThe Journal of experimental medicine2003
Antiadhesive role of apical decay-accelerating factor (CD55) in human neutrophil transmigration across mucosal epithelia.
Article in The Journal of experimental medicine, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
44 citing papers in PubMed, 78 citations in OpenAlex.
- Persistent pneumococcal colonisation in antiretroviral-treated HIV infection is associated with nasal inflammation.Nature communications · 2025Article
- Contact-dependent, polarized acidification response during neutrophil-epithelial interactions.Journal of leukocyte biology · 2022Article
- LEUKOCYTE-EPITHELIAL INTERACTIONS: A DOUBLE-EDGED SWORD THAT PROTECTS AND INJURES DURING HEALTH AND DISEASE.Transactions of the American Clinical and Climatological Association · 2022Article
- Regulatory mechanisms of neutrophil migration from the circulation to the airspace.Cellular and molecular life sciences : CMLS · 2021Review
- The Glycoprotease CpaA Secreted by Medically Relevant Acinetobacter Species Targets MultiplemBio · 2020Article
- The HIF target ATG9A is essential for epithelial barrier function and tight junction biogenesis.Molecular biology of the cell · 2020Article
- Effect of vitamin E on stroke-associated pneumonia.The Journal of international medical research · 2020Article
- Resolvin E1 is a pro-repair molecule that promotes intestinal epithelial wound healing.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Plasma membrane profiling during enterohemorrhagicThe Journal of biological chemistry · 2018Article
- Neutrophils as sources of dinucleotide polyphosphates and metabolism by epithelial ENPP1 to influence barrier function via adenosine signaling.Molecular biology of the cell · 2018Article
- Special pro-resolving mediator (SPM) actions in regulating gastro-intestinal inflammation and gut mucosal immune responses.Molecular aspects of medicine · 2017Review
- Neutrophils as Components of Mucosal Homeostasis.Cellular and molecular gastroenterology and hepatology · 2017Review
- 4-Aroyl-3-hydroxy-5-phenyl-1H-pyrrol-2(5H)-ones as N-formyl peptide receptor 1 (FPR1) antagonists.Biochemical pharmacology · 2017Article
- Protection of host cells by complement regulators.Immunological reviews · 2016Review
- Pathobiology of neutrophil-epithelial interactions.Immunological reviews · 2016Review
- Neutrophil interactions with epithelial-expressed ICAM-1 enhances intestinal mucosal wound healing.Mucosal immunology · 2016Article
- Neutrophil-Epithelial Interactions: A Double-Edged Sword.The American journal of pathology · 2016Review
- Euphorbia tirucalli modulates gene expression in larynx squamous cell carcinoma.BMC complementary and alternative medicine · 2016Article
- Targeting of Neutrophil Lewis X Blocks Transepithelial Migration and Increases Phagocytosis and Degranulation.The American journal of pathology · 2016Article
- Specialized pro-resolving mediators: endogenous regulators of infection and inflammation.Nature reviews. Immunology · 2016Review
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 3 institutions in 1 country.
Funding
Abstract
Neutrophil migration across mucosal epithelium during inflammatory episodes involves the precise orchestration of a number a cell surface molecules and signaling pathways. After successful migration to the apical epithelial surface, apically localized epithelial proteins may serve to retain PMN at the lumenal surface. At present, identification of apical epithelial ligands and their PMN counter-receptors remain elusive. Therefore, to define the existence of apical epithelial cell surface proteins involved in PMN-epithelial interactions, we screened a panel of antibodies directed against epithelial plasma membranes. This strategy identified one antibody (OE-1) that both localized to the apical cell membrane and significantly inhibited PMN transmigration across epithelial monolayers. Microsequence analysis revealed that OE-1 recognized human decay-accelerating factor (DAF, CD55). DAF is a highly glycosylated, 70-80-kD, glycosyl-phosphatidyinositol-linked protein that functions predominantly as an inhibitor of autologous complement lysis. DAF suppression experiments using antisense oligonucleotides or RNA interference revealed that DAF may function as an antiadhesive molecule promoting the release of PMN from the lumenal surface after transmigration. Similarly, peptides corresponding to the antigen recognition domain of OE-1 resulted in accumulation of PMN on the apical epithelial surface. The elucidation of DAF as an apical epithelial ligand for PMN provides a target for novel anti-inflammatory therapies directed at quelling unwanted inflammatory episodes.
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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.