ArticleJournal of the Formosan Medical Association = Taiwan yi zhi2022
Innate immune response analysis in COVID-19 and kawasaki disease reveals MIS-C predictors.
Article in Journal of the Formosan Medical Association = Taiwan yi zhi, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 30 citations in OpenAlex.
- Pattern Recognition Receptors (PRRs) Expression and Activation in COVID-19 and Long COVID: From SARS-CoV-2 Escape Mechanisms to Emerging PRR-Targeted Immunotherapies.Microorganisms · 2025Review
- The X-LinkedInternational journal of molecular sciences · 2025Article
- Tissue inflammation induced by constitutively active STING is mediated by enhanced TNF signaling.eLife · 2025Article
- Cytosolic nucleic acid sensing as driver of critical illness: mechanisms and advances in therapy.Signal transduction and targeted therapy · 2025Review
- Review
- Progress on diagnosis and treatment of multisystem inflammatory syndrome in children.Frontiers in immunology · 2025Review
- Virus-specific host responses and gene signatures following infection with major SARS-CoV-2 variants of concern: role of ZBP1 in viral clearance and lung inflammation.Frontiers in immunology · 2025Article
- The causal association between COVID-19 and ischemic stroke: a mendelian randomization study.Virology journal · 2024Article
- Immunity and Coagulation in COVID-19.International journal of molecular sciences · 2024Review
- The plasma proteome differentiates the multisystem inflammatory syndrome in children (MIS-C) from children with SARS-CoV-2 negative sepsis.Molecular medicine (Cambridge, Mass.) · 2024Article
- Inflammasome-Related Genetic Polymorphisms as Severity Biomarkers of COVID-19.International journal of molecular sciences · 2024Article
- Nucleic acid biomarkers of immune response and cell and tissue damage in children with COVID-19 and MIS-C.Cell reports. Medicine · 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
- Immunogenic cell death-led discovery of COVID-19 biomarkers and inflammatory infiltrates.Frontiers in microbiology · 2023Article
- Toll-Like Receptor Signaling in Severe Acute Respiratory Syndrome Coronavirus 2-Induced Innate Immune Responses and the Potential Application Value of Toll-Like Receptor Immunomodulators in Patients With Coronavirus Disease 2019.Frontiers in microbiology · 2022Review
- Involvement of the STING signaling in COVID-19.Frontiers in immunology · 2022Review
- Progress of cGAS-STING signaling in response to SARS-CoV-2 infection.Frontiers in immunology · 2022Review
- Case Report: Ciclosporin A for Refractory Multisystem Inflammatory Syndrome in Children.Frontiers in pediatrics · 2022Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background/purposeThe association between dysregulated innate immune responses seen in Kawasaki disease (KD) with predisposition to Kawasaki-like multisystem inflammatory syndrome in children (MIS-C) remains unclear. We aimed to compare the innate immunity transcriptome signature between COVID-19 and KD, and to analyze the interactions of these molecules with genes known to predispose to KD.
methodsTranscriptome datasets of COVID-19 and KD cohorts (E-MTAB-9357, GSE-63881, GSE-68004) were downloaded from ArrayExpress for innate immune response analyses. Network analysis was used to determine enriched pathways of interactions.
resultsUpregulations of IRAK4, IFI16, STING, STAT3, PYCARD, CASP1, IFNAR1 and CD14 genes were observed in blood cells of acute SARS-CoV-2 infections with moderate severity. In the same patient group, increased expressions of TLR2, TLR7, IRF3, and CD36 were also noted in blood drawn a few days after COVID-19 diagnosis. Elevated blood PYCARD level was associated with severe COVID-19 in adults. Similar gene expression signature except differences in TLR8, NLRP3, STING and IRF3 levels was detected in KD samples. Network analysis on innate immune genes and genes associated with KD susceptibility identified enriched pathways of interactions. Furthermore, higher expression levels of KD susceptibility genes HLA-DOB, PELI1 and FCGR2A correlated with COVID-19 of different severities.
conclusionOur findings suggest that most enriched innate immune response pathways were shared between transcriptomes of KD and COVID-19 with moderate severity. Genetic polymorphisms associated with innate immune dysregulation and KD susceptibility, together with variants in STING and STAT3, might predict COVID-19 severity and potentially susceptibility to COVID-19 related MIS-C.
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