Exploration of common genomic signatures of systemic juvenile idiopathic arthritis and Kawasaki disease

The findings of this study provide substantial evidence of the complex and dynamic immune system abnormalities underlying SJIA and KD. A common pathogenic mechanism may involve TNF activity, neutrophil degranulation, and the NF-kB pathway. Additionally, a more detailed investigation into the regulatory roles of EGR1, BCL6, FOS, and NFE2 within this network is essential. Key Points • The study retrieved and analyzed microarray data for both conditions from the Gene Expression Omnibus (GEO) database，to investigate the common genetic patterns and potential molecular processes involved in systemic juvenile idiopathic arthritis (SJIA) and Kawasaki disease (KD). • The study identified a total of 204 upregulated and 35 downregulated SDEGs. A network targeting transcription factors revealed four specific TFs (EGR1, 20BCL6, FOS, and NFE2), which were further examined. • The findings of this study provide substantial evidence of the complex and dynamic immune system abnormalities underlying SJIA and KD. A common pathogenic mechanism may involve TNF activity, neutrophil degranulation, and the NF-kB pathway.