ArticlePloS one2010
Association of CCR2-CCR5 haplotypes and CCL3L1 copy number with Kawasaki Disease, coronary artery lesions, and IVIG responses in Japanese children.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Pooled it
- T-cadherin deprivation in endothelial cells promotes vascular injury in Kawasaki disease through SOD2/ROS/NLRP3 pathway-mediated pyroptosis.Journal of molecular cell biology · 2026Article
- Endothelial Dysfunction: Molecular Mechanisms and Therapeutic Strategies in Kawasaki Disease.International journal of molecular sciences · 2024Review
- Predictive model based on gene and laboratory data for intravenous immunoglobulin resistance in Kawasaki disease in a Chinese population.Pediatric rheumatology online journal · 2021Article
- Association between P2RY12 Gene Polymorphisms and IVIG Resistance in Kawasaki Patients.Cardiovascular therapeutics · 2020Article
- Translational Metabolomics: Current Challenges and Future Opportunities.Metabolites · 2019Article
- Leveraging Genetic Findings for Precision Medicine in Vasculitis.Frontiers in immunology · 2019Review
- Review: Found in Translation: International Initiatives Pursuing Interleukin-1 Blockade for Treatment of Acute Kawasaki Disease.Arthritis & rheumatology (Hoboken, N.J.) · 2017Review
- Complex and multi-allelic copy number variation in human disease.Briefings in functional genomics · 2015Review
- Imputation of class I and II HLA loci using high-density SNPs from ImmunoChip and their associations with Kawasaki disease in family-based study.International journal of immunogenetics · 2015Article
- CCL3L1 copy number, HIV load, and immune reconstitution in sub-Saharan Africans.BMC infectious diseases · 2013Article
- Complete haplotype sequence of the human immunoglobulin heavy-chain variable, diversity, and joining genes and characterization of allelic and copy-number variation.American journal of human genetics · 2013Article
- Can Coronary Artery Involvement in Kawasaki Disease be Predicted?Diagnostics (Basel, Switzerland) · 2013Review
- Understanding the pathogenesis of Kawasaki disease by network and pathway analysis.Computational and mathematical methods in medicine · 2013Review
- Variations in the number of CCL3L1 gene copies and Kawasaki disease in Korean children.Pediatric cardiology · 2012Article
- Cardiovascular genomics: a biomarker identification pipeline.IEEE transactions on information technology in biomedicine : a publication of the IEEE Engineering in Medicine and Biology Society · 2012Review
- Exploring the potential relevance of human-specific genes to complex disease.Human genomics · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 9 institutions in 2 countries.
Funding
Abstract
backgroundThe etiology of Kawasaki Disease (KD) is enigmatic, although an infectious cause is suspected. Polymorphisms in CC chemokine receptor 5 (CCR5) and/or its potent ligand CCL3L1 influence KD susceptibility in US, European and Korean populations. However, the influence of these variations on KD susceptibility, coronary artery lesions (CAL) and response to intravenous immunoglobulin (IVIG) in Japanese children, who have the highest incidence of KD, is unknown. METHODOLOGY/PRINCIPAL
findingsWe used unconditional logistic regression analyses to determine the associations of the copy number of the CCL3L1 gene-containing duplication and CCR2-CCR5 haplotypes in 133 Japanese KD cases [33 with CAL and 25 with resistance to IVIG] and 312 Japanese controls without a history of KD. We observed that the deviation from the population average of four CCL3L1 copies (i.e., <or>four copies) was associated with an increased risk of KD and IVIG resistance (adjusted odds ratio (OR)=2.25, p=0.004 and OR=6.26, p=0.089, respectively). Heterozygosity for the CCR5 HHF*2 haplotype was associated with a reduced risk of both IVIG resistance (OR=0.21, p=0.026) and CAL development (OR=0.44, p=0.071). CONCLUSIONS/SIGNIFICANCE: The CCL3L1-CCR5 axis may play an important role in KD pathogenesis. In addition to clinical and laboratory parameters, genetic markers may also predict risk of CAL and resistance to IVIG.
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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.