ReviewFrontiers in immunology2025
Polymorphism-driven immune disruptions in Kawasaki disease across populations: decoding the role of T and B-cells.
Review in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- The Autophagy-Inflammasome Axis as a Molecular Switch: From Persistent Inflammation to Vascular Remodeling in IVIG-Resistant Kawasaki Disease.International journal of molecular sciences · 2026Review
- From acute immune storm to lifelong vascular risk: a paradigm shift in Kawasaki disease as a chronic disease model.Frontiers in pediatrics · 2026Article
- Kawasaki Disease: Unraveling Immunopathogenesis, Genetic Factors, and AI Applications in Diagnosis with a Focus on Iran.Pediatric cardiology · 2025Review
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kawasaki disease (KD) is a self-limiting, systemic vasculitic syndrome of unknown etiology that primarily affects children under the age of five, with notably high incidence in Asian populations. Although initial treatment with high-dose intravenous immunoglobulin (IVIG) and aspirin can reduce acute symptoms of KD and the risk of coronary artery lesions (CALs), diagnosis remains challenging due to the absence of specific biomarkers and the incomplete understanding of disease pathogenesis, often resulting in misdiagnosis or delayed intervention. Genetic predisposition and immune dysregulation, particularly involving B-cell and T-cell pathways, have been implicated in KD susceptibility and the development of CAL. This review summarizes current evidence on immune-regulatory gene polymorphisms, with a focus on how T-cell and B-cell-related genetic variations may contribute to disease onset and vascular complications. These insights may help inform improved diagnostic accuracy-particularly for incomplete KD-and support personalized treatment strategies, such as corticosteroids or anti-TNF agents in genetically high-risk patients.
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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 Socratic graph.