# Identification of potential biomarkers associated with immune cell infiltration patterns in Kawasaki disease via bioinformatics

**Authors:** Guolian Wu, Hui Liu, Meiling Wang, Rong Wang, Xiaosheng Tan, Xiaosheng Tan, Xiaosheng Tan

PMC · DOI: 10.1371/journal.pone.0324337 · PLOS One · 2025-06-02

## TL;DR

This study identifies key genes and immune cell patterns in Kawasaki disease, offering potential biomarkers for diagnosis and treatment.

## Contribution

The study introduces five hub genes and immune infiltration patterns specific to Kawasaki disease using bioinformatics.

## Key findings

- Five hub genes (AURKB, BUB1, CCL2, IL-4, and TOP2A) were identified as potential biomarkers for Kawasaki disease.
- Immune cell infiltration analysis showed increased monocytes and neutrophils, but decreased B and T cells in KD patients.
- The DEGs were linked to inflammation, immune response, and signaling pathways like PI3K-Akt and cytokine interactions.

## Abstract

Inflammation and immune dysregulation play critical roles in Kawasaki disease (KD) pathogenesis, yet specific biomarkers and immune signatures remain elusive. This study aims to identify key biomarkers and characterize immune cell infiltration scores in KD using bioinformatic approaches. The GSE73461 dataset, downloaded from the Gene Expression Omnibus (GEO) database, includes 78 KD patients and 55 normal controls collected by Imperial College London from 2015 to 2023, and was analyzed to identify differentially expressed genes (DEGs). Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis revealed significant involvement of these DEGs in acute inflammatory responses, plasma membrane components, PI3K-Akt signaling, and cytokine interactions. Protein-protein interaction (PPI) network was constructed, and five candidate hub genes (AURKB, BUB1, CCL2, IL-4, and TOP2A) were identified. Immune cell infiltration analysis gusing the XCell algorithm showed increased levels of Monocytes, neutrophils, and other immune cells in KD, while B cells and T cells were decreased. Correlation analysis indicated that these candidate hub genes are associated with immune dysregulation and inflammation in KD. These findings provide potential diagnostic biomarkers and therapeutic targets for KD, warranting further validation in larger studies.

## Linked entities

- **Genes:** AURKB (aurora kinase B) [NCBI Gene 9212], BUB1 (BUB1 mitotic checkpoint serine/threonine kinase) [NCBI Gene 699], CCL2 (C-C motif chemokine ligand 2) [NCBI Gene 6347], IL4 (interleukin 4) [NCBI Gene 3565], TOP2A (DNA topoisomerase II alpha) [NCBI Gene 7153]
- **Diseases:** Kawasaki disease (MONDO:0012727)

## Full-text entities

- **Genes:** TOP2A (DNA topoisomerase II alpha) [NCBI Gene 7153] {aka TOP2, TOP2alpha, TOPIIA, TP2A}, AURKB (aurora kinase B) [NCBI Gene 9212] {aka AIK2, AIM-1, AIM1, ARK-2, ARK2, AurB}, IL4 (interleukin 4) [NCBI Gene 3565] {aka BCGF-1, BCGF1, BSF-1, BSF1, IL-4}, CCL2 (C-C motif chemokine ligand 2) [NCBI Gene 6347] {aka GDCF-2, HC11, HSMCR30, MCAF, MCP-1, MCP1}, PIK3CB (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit beta) [NCBI Gene 5291] {aka P110BETA, PI3K, PI3KBETA, PIK3C1}, AKT1 (AKT serine/threonine kinase 1) [NCBI Gene 207] {aka AKT, PKB, PKB-ALPHA, PRKBA, RAC, RAC-ALPHA}, BUB1 (BUB1 mitotic checkpoint serine/threonine kinase) [NCBI Gene 699] {aka BUB1A, BUB1L, MCPH30, hBUB1}
- **Diseases:** Inflammation (MESH:D007249), immune dysregulation (OMIM:614878), KD (MESH:D009080)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12129191/full.md

## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12129191/full.md

## References

42 references — full list in the complete paper: https://tomesphere.com/paper/PMC12129191/full.md

---
Source: https://tomesphere.com/paper/PMC12129191