ObjectiveTo preliminarily investigate the potential role and mechanism of N6-methyladenosine (m6A) regulators in the immune microenvironment of ischemic stroke (IS). MethodsBased on the Gene Expression Omnibus (GEO) database, the correlation between m6A regulators and the IS immune microenvironment was comprehensively analyzed by using bioinformatics methods such as single-sample gene set enrichment analysis (ssGSEA), consistency cluster analysis, and gene set enrichment analysis (GSEA). ResultsThe results of Spearman correlation analysis showed that the expression of IGF2BP2 mRNA had the strongest positive correlation with the enrichment score of CD56 bright natural killer cells (rs=0.66), and the expression of IGF2BP2 mRNA had the strongest negative correlation with the enrichment score of type 2 T helper cells (rs=-0.64). The expression of ELF3 mRNA had the strongest positive correlation with the enrichment score of TGFb family members (rs=0.56), and the expression of ELAVL1 mRNA had the strongest negative correlation with the enrichment score of chemokines (rs=-0.66) (all P＜0.05). The consistency clustering analysis identified two IS subtypes with different m6A modification patterns, subtype 1 had higher enrichment scores of activated B cells, activated CD4 T cells, activated CD8 T cells, effector memory CD8 T cells, natural killer T cells, type 2 T helper cells, interleukins, and TCR signaling pathway, but lower enrichment scores of activated dendritic cells, CD56 bright natural killer cells, plasmacytoid dendritic cells, TGFb family members, and TNF family members compared with subtype 2(all P＜0.05). The results of GSEA indicated that subtype 2 may be dynamically correlated to signaling pathways such as olfactory transduction, tight junction, and leukocyte transendothelial migration. ConclusionThere is a correlation between m6A modification and the IS immune microenvironment.

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