ArticleMolecular and cellular biochemistry2016
Interleukin-27 enhances TNF-α-mediated activation of human coronary artery endothelial cells.
Article in Molecular and cellular biochemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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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
20 citing papers in PubMed, 30 citations in OpenAlex.
- Prognostic Impact of Interleukin-27 in Peripheral Artery Disease.Life (Basel, Switzerland) · 2025Article
- Recent Insights Into Targeting Interleukin-27 in Coronary Artery Disease.Journal of cardiovascular translational research · 2025Review
- Analysis and validation of hub genes for atherosclerosis and AIDS and immune infiltration characteristics based on bioinformatics and machine learning.Scientific reports · 2025Article
- Exploring the Involvement of New Members of the Interleukin Family in Cardiovascular Disease.Current cardiology reviews · 2025Review
- Association between Plasma Interleukin-27 Levels and Cardiovascular Events in Patients Undergoing Coronary Angiography.Journal of cardiovascular development and disease · 2024Article
- Article
- Signal Transduction and Gene Regulation in the Endothelium.Cold Spring Harbor perspectives in medicine · 2023Review
- Article
- Review
- Tregs-derived interleukin 35 attenuates endothelial proliferation through STAT1 in pulmonary hypertension.Annals of translational medicine · 2021Article
- Elevated Levels of Interleukin-27 in Early Life Compromise Protective Immunity in a Mouse Model of Gram-Negative Neonatal Sepsis.Infection and immunity · 2020Article
- Plasma levels of interleukin 27 in falciparum malaria is increased independently of co-infection with HIV: potential immune-regulatory role during malaria.BMC infectious diseases · 2020Article
- Laquinimod Protects Against TNF-α-Induced Attachment of Monocytes to Human Aortic Endothelial Cells (HAECs) by Increasing the Expression of KLF2.Drug design, development and therapy · 2020Article
- The interleukin-27 -964A>G polymorphism enhances sepsis-induced inflammatory responses and confers susceptibility to the development of sepsis.Critical care (London, England) · 2018Article
- Increased IL-27/IL-27R expression in association with the immunopathology of murine ocular toxoplasmosis.Parasitology research · 2018Article
- Atherogenic dyslipidemia promotes autoimmune follicular helper T cell responses via IL-27.Nature immunology · 2018Article
- Observational
- Interleukin 27 is increased in carotid atherosclerosis and promotes NLRP3 inflammasome activation.PloS one · 2017Article
- CC-Chemokine Ligand 2 (CCL2) Suppresses High Density Lipoprotein (HDL) Internalization and Cholesterol Efflux via CC-Chemokine Receptor 2 (CCR2) Induction and p42/44 Mitogen-activated Protein Kinase (MAPK) Activation in Human Endothelial Cells.The Journal of biological chemistry · 2016Article
- The CXCL10/CXCR3 Axis and Cardiac Inflammation: Implications for Immunotherapy to Treat Infectious and Noninfectious Diseases of the Heart.Journal of immunology research · 2016Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immune cells and inflammatory mediators play important roles in the development of atherosclerotic vascular inflammation. IL-27 is a member of the IL-6/IL-12 family that can promote Th1 responses and augment the release of inflammatory mediators from human mast cells and monocytes. However, the direct effect of IL-27 on human coronary artery endothelial cells was unclear. In this study, the effects of IL-27 and TNF-α on the cell surface expression of adhesion molecules, inflammatory cytokines, and chemokines were investigated. Results showed that IL-27 alone could significantly promote the release of chemokine CXCL10. However, IL-27 could further significantly enhance the TNF-α-mediated upregulation of adhesion molecules ICAM-1 and VCAM-1, inflammatory cytokine IL-6, as well as chemokines CCL5 and CXCL10 from human coronary artery endothelial cells. The release of IL-6, CCL5, and CXCL10 were significantly suppressed by specific signaling molecule inhibitors, implying that the induction of these mediators from the human coronary artery endothelial cells could be differentially regulated by the c-Jun N-terminal kinase, p38 mitogen-activated protein kinase, and nuclear factor-κB pathways. These results provided new insights into the effect of IL-27 on the TNF-α mediated activation of human coronary artery endothelial cells in atherosclerotic vascular inflammation.
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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.