ArticleOncotarget2017
Identifying genetic hypomethylation and upregulation of Toll-like receptors in Kawasaki disease.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.
- Phenotype, Susceptibility, Autoimmunity, and Immunotherapy Between Kawasaki Disease and Coronavirus Disease-19 Associated Multisystem Inflammatory Syndrome in Children.Frontiers in immunology · 2021Pooled it
- Fertility Treatments and the Risk of Kawasaki Disease Among Offspring.JAMA network open · 2026Article
- Combination of S100A12/TLR2 signaling molecules and clinical indicators in a new predictive model for IVIG-resistant Kawasaki disease.Scientific reports · 2024Article
- NLRC4 methylation and its response to intravenous immunoglobulin therapy in Kawasaki disease: a case control study.BMC pediatrics · 2024Article
- Preliminary Evidence of the Differential Expression of Human Endogenous Retroviruses in Kawasaki Disease and SARS-CoV-2-Associated Multisystem Inflammatory Syndrome in Children.International journal of molecular sciences · 2023Article
- From Co-Infections to Autoimmune Disease via Hyperactivated Innate Immunity: COVID-19 Autoimmune Coagulopathies, Autoimmune Myocarditis and Multisystem Inflammatory Syndrome in Children.International journal of molecular sciences · 2023Review
- Article
- G0S2 regulates innate immunity in Kawasaki disease via lncRNA HSD11B1-AS1.Pediatric research · 2022Article
- The Role of E3 Ligase Pirh2 in Disease.Cells · 2022Review
- Human Transcriptome Array Analysis Identifies CDR2 as a Novel Suppressed Gene for Kawasaki Disease.Diagnostics (Basel, Switzerland) · 2022Article
- CD36 is Associated With the Development of Coronary Artery Lesions in Patients With Kawasaki Disease.Frontiers in immunology · 2022Article
- Epigenetic regulation of pediatric and neonatal immune responses.Pediatric research · 2022Review
- Comparable bidirectional neutrophil immune dysregulation between Kawasaki disease and severe COVID-19.Frontiers in immunology · 2022Article
- KDmarkers: A biomarker database for investigating epigenetic methylation and gene expression levels in Kawasaki disease.Computational and structural biotechnology journal · 2022Article
- Increased Expression of Pyroptosis in Leukocytes of Patients with Kawasaki Disease.Diagnostics (Basel, Switzerland) · 2021Article
- Prognostic Impact of Genetic Variants of MECP2 and TIRAP on Clinical Outcomes of Systemic Lupus Erythematosus with and without Nephritis.Biomolecules · 2021Article
- Public Health Interventions for COVID-19 Reduce Kawasaki Disease in Taiwan.Children (Basel, Switzerland) · 2021Article
- Identification of Key Genes and Underlying Mechanisms in Acute Kawasaki Disease Based on Bioinformatics Analysis.Medical science monitor : international medical journal of experimental and clinical research · 2021Article
- Perspective of Immunopathogenesis and Immunotherapies for Kawasaki Disease.Frontiers in pediatrics · 2021Review
- Epigenetics in Kawasaki Disease.Frontiers in pediatrics · 2021Review
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kawasaki disease (KD) is an acute febrile systemic vasculitis that occurs in children and is characterized by elevated levels of proinflammatory cytokines. Toll-like receptors (TLRs) serve as the sensor arm of the innate immune system and induce proinflammatory cytokine expressions.We recruited a total of 18 paired KD patients, before intravenous immunoglobulin (IVIG) and at least 3 weeks after IVIG treatment, 18 healthy controls, and 18 febrile controls. For TLR genes and their cytosine-phosphate-guanine (CpG) markers, we used Affymetrix GeneChip® Human Transcriptome Array 2.0 and Illumina HumanMethylation450 BeadChip to evaluate gene expression levels and methylation patterns, respectively.KD patients demonstrated a significantly differential expression of TLR mRNA levels compared to both the healthy and febrile controls, with only TLR 3 and 7 not differing between the KD patients and the controls. After patients underwent IVIG treatment, the TLR mRNA levels, except for TLR3, decreased significantly in KD patients. In contrast, the methylation status of the CpG sites of TLR1, 2, 4, 6, 8, and 9 demonstrated an opposite tendency between the two stages of both the KD samples and the controls.TLRs, particularly TLR1, 2, 4, 6, 8, and 9, may stimulate the immunopathogenesis of KD. These results are among the first to use TLRs to prove that a bacterial inflammatory response may trigger KD.
Indexed as
Identifiers
What OpenQuestion holds
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.