ArticleJournal of translational medicine2008
Interdependency of CEACAM-1, -3, -6, and -8 induced human neutrophil adhesion to endothelial cells.
Article in Journal of translational medicine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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
39 citing papers in PubMed, 63 citations in OpenAlex.
- Gene expression profiling of whole blood in ipilimumab-treated patients for identification of potential biomarkers of immune-related gastrointestinal adverse events.Journal of translational medicine · 2013Trial
- Trial
- Mechanism of AGEs-RAGE axis inhibition of ferroptosis in type 2 diabetic colon cancer by regulatory CEACAM1.Scientific reports · 2026Article
- Expression of Human CEACAM Receptors Promotes Inflammation and Organ Damage During SystemicCells · 2026Article
- Sitagliptin Modulates Functional and Phenotypic Properties of Human Neutrophils Under Normal- and High-Glucose Conditions In Vitro.Molecules (Basel, Switzerland) · 2026Article
- Article
- CEACAM1 in vascular homeostasis and inflammation.European journal of clinical investigation · 2024Review
- The role of CEACAMs in neutrophil function.European journal of clinical investigation · 2024Review
- Prognostic heterogeneity of Ki67 in non-small cell lung cancer: A comprehensive reappraisal on immunohistochemistry and transcriptional data.Journal of cellular and molecular medicine · 2024Article
- CEACAM6 expression and function in tumor biology: a comprehensive review.Discover oncology · 2024Review
- Identification and validation of aging-related genes in neuropathic pain using bioinformatics.Frontiers in genetics · 2024Article
- CEACAM expression in anFrontiers in immunology · 2023Article
- Old and New Blood Markers in Human Colorectal Cancer.International journal of molecular sciences · 2022Review
- Low Density Granulocytes and Dysregulated Neutrophils Driving Autoinflammatory Manifestations in NEMO Deficiency.Journal of clinical immunology · 2022Article
- An investigation into the role of inherited CEACAM gene family variants and colorectal cancer risk.BMC research notes · 2022Article
- Article
- CEACAM 1, 3, 5 and 6 -positive classical monocytes correlate with interstitial lung disease in early systemic sclerosis.Frontiers in immunology · 2022Article
- The Visualization of Protein-Protein Interactions in Breast Cancer: Deployment Study in Pathological Examination.Acta histochemica et cytochemica · 2021Review
- Neutrophil Pathways of Inflammation Characterize the Blood Transcriptomic Signature of Patients with Psoriasis and Cardiovascular Disease.International journal of molecular sciences · 2021Article
- Single-cell transcriptomics reveals the landscape of intra-tumoral heterogeneity and transcriptional activities of ECs in CC.Molecular therapy. Nucleic acids · 2021Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Members of the carcinoembryonic antigen family (CEACAMs) are widely expressed, and, depending on the tissue, capable of regulating diverse functions including tumor promotion, tumor suppression, angiogenesis, and neutrophil activation. Four members of this family, CEACAM1, CEACAM8, CEACAM6, and CEACAM3 (recognized by CD66a, CD66b, CD66c, and CD66d mAbs, respectively), are expressed on human neutrophils. CD66a, CD66b, CD66c, and CD66d antibodies each increase neutrophil adhesion to human umbilical vein endothelial cell monolayers. This increase in neutrophil adhesion caused by CD66 antibodies is blocked by CD18 mAbs and is associated with upregulation of CD11/CD18 on the neutrophil surface. To examine potential interactions of CEACAMs in neutrophil signaling, the effects on neutrophil adhesion to human umbilical vein endothelial cells of a set of CD66 mAbs was tested following desensitization to stimulation by various combinations of these mAbs. Addition of a CD66 mAb in the absence of calcium results in desensitization of neutrophils to stimulation by that CD66 mAb. The current data show that desensitization of neutrophils to any two CEACAMs results in selective desensitization to those two CEACAMs, while the cells remain responsive to the other two neutrophil CEACAMs. In addition, cells desensitized to CEACAM-3, -6, and -8 were still responsive to stimulation of CEACAM1 by CD66a mAbs. In contrast, desensitization of cells to CEACAM1 and any two of the other CEACAMs left the cells unresponsive to all CD66 mAbs. Cells desensitized to any combination of CEACAMs remained responsive to the unrelated control protein CD63. Thus, while there is significant independence of the four neutrophil CEACAMs in signaling, CEACAM1 appears to play a unique role among the neutrophil CEACAMs. A model in which CEACAMs dimerize to form signaling complexes could accommodate the observations. Similar interactions may occur in other cells expressing CEACAMs.
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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.