Abstract
Objective: Kawasaki Disease (KD) is the primary cause of acquired heart disease among children in developed countries and is identified by systemic vasculitis of unknown origin. This research explores the possible common pathogenesis between KD and coronavirus disease 2019 (COVID-19), focusing on the roles of peripheral blood mononuclear cell (PBMC) subpopulations. Methods: We utilized single-cell and bulk RNA sequencing data from COVID-19 and KD patients, as well as healthy controls. Our comprehensive analysis included cell-type identification, pseudotime analysis, cell-cell communication, and transcription factor analysis. Results: Our results show the critical role of CD4+ effector memory T cells and dendritic cells in the autoimmune pathology of COVID-19 and KD. These cells interact through specific signaling pathways, including MIF, IL16, and FLT3. Notably, the transcription factor IKZF1, which is observed to increase IL16 expression, connects CD4+ effector memory T cells with dendritic cell activation, playing a significant role in inflammatory responses. Conclusion: The study highlights the intricate immune interactions in KD and COVID-19, indicating potential new therapeutic targets to address the autoimmune pathologies linked with these conditions.
Recommended Citation
Yan, Seyan; Zheng, Kaiming; Zhen, Zicheng; and Xu, Tianfu
(2025)
"Modulation of Dendritic Cell Phenotypes by CD4+ Effector Memory T Cell via IKZF1-Regulated IL16/CD4 Signaling in COVID-19 and Kawasaki Disease,"
Journal of Pediatric Infectious Diseases: Vol. 20:
Iss.
3, Article 9.
Available at:
https://jpid.researchcommons.org/journal/vol20/iss3/9