Objective: To investigate the pathogenesis of idiopathic thrombocytopenic purpura(ITP) in children based on bioinformatics technology. Methods: In this study, we obtained microarray data related to childhood ITP by searching the Gene Expression Omnibus database, and screened the differentially expressed genes(DEGs) between children with ITP and normal children by using the GEO2R online analysis tool. The obtained DEGs were subjected to GO annotation and KEGG pathway enrichment analysis through the DAVID data website, and the protein interaction network(PPT) was constructed and analyzed for core targets using the STRING database and Cytoscape software. Finally, gene set enrichment analysis(GSEA) and immune cell infiltration analysis(ICI) were performed on the microarray data set. Results: 276 DEGs were obtained, of which 191 were up-regulated and 85 were down-regulated. GO analysis showed that DEGs were mainly enriched in cell matrix adhesion, negative regulation of mast cell activation, extracellular matrix organization, and hemoglobin complex. KEGG analysis showed enrichment in inhibitors of receptor tyrosine kinases, ErbB signaling pathway, Rap1 signaling pathway axon guidance, PI3K-Akt signaling pathway, and complement and coagulation systems. GSEA analysis showed significant enrichment in neural signaling pathways, melanoma, extracellular matrix receptor interactions, regulation of the actin cytoskeleton, and adhesive plaques. ICI analysis suggested an increase in the relative content of M2 macrophages and follicular helper T cells in the ITP group, activated dendritic cells and resting memory CD4+ T cells were reduced. Conclusion: The pathogenesis of ITP in children may be due to abnormal expression of genes such as ITGB3, ARRB1, COL3A1, COL11A1, and CFTR through biological processes such as neuroactive ligand-receptor interactions, integrin receptor binding, cell adhesion regulation, and mediation of ErbB and PI3K-Akt signaling pathways thereby causing immune cell abnormal expression and reduction of platelets.
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