# TCR Repertoire Analysis Unveils the Link Between Kawasaki Disease and Viral Infection

## TL;DR

This study uses T cell receptor analysis to explore the connection between Kawasaki disease and viral infections, finding distinct immune patterns in patients.

## Contribution

The study identifies unique TCR motifs and diversity patterns in Kawasaki disease, suggesting a potential link to viral infections.

## Key findings

- KD patients showed reduced TCR clonal abundance and diversity compared to healthy controls.
- A specific TCR combination with characteristic amino acid motifs was frequently found in KD patients.
- Limited overlap in clonal TCRαβ chains was observed between KD and viral infection groups.

## Abstract

Background: Kawasaki disease (KD) is a systemic vasculitis of unknown origin, though recent evidence implicates viral pathogens in its pathogenesis. Given the central role of T cell receptors (TCRs) in antigen recognition and immune response, this study investigated the association between KD and viral infection through comparative analysis of TCR repertoires. Methods: TCR repertoires from KD patients, healthy children, and individuals with viral infections were comparatively analyzed. TCR diversity and V(D)J usage were assessed using Shannon’s entropy, the Mann–Whitney U test, and Fisher’s exact test. Positional motif enrichment analysis within CDR3 regions was performed based on paratope hotspot classification. Results: Relatively reduced TCR clonal abundance and diversity were observed in KD patients compared to healthy controls. While substantial overlap in VJ gene segment usage was detected between KD and cytomegalovirus (CMV) infection, limited overlap in clonal TCRαβ chains was found between KD and viral infection groups. A predominant TCR combination, TRAV14DV4-J13-TRBV20-1-J2-5, enriched with characteristic amino acid motifs (EET, YNE, LAG, GQG, and AYE), was frequently identified in KD. Conclusions: These observations suggest potential differences in TCR repertoire features between KD patients and both healthy and virus-infected groups. However, the relationship between KD pathogenesis and the viruses examined requires further investigation with larger cohorts.