# Polymorphism-driven immune disruptions in Kawasaki disease across populations: decoding the role of T and B-cells

## TL;DR

This paper reviews how genetic variations in immune cells may contribute to Kawasaki disease, offering insights for better diagnosis and personalized treatment.

## Contribution

The paper highlights novel insights into how T-cell and B-cell gene polymorphisms influence Kawasaki disease susceptibility and complications.

## Key findings

- Genetic variations in T-cell and B-cell pathways are linked to Kawasaki disease susceptibility.
- Immune-regulatory gene polymorphisms may explain differences in disease severity and coronary artery lesions.
- Understanding these polymorphisms could improve diagnosis and guide personalized therapies.

## 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.