Objective: To identify characteristic genes of rheumatoid arthritis (RA) by artificial neural network and to analyze role of immune cells in RA related microenvironment. Methods: GSE1919 and GSE77298 chips were from GEO database. Two chips were combined and batch corrected using R language to obtain a new data set, and difference was analyzed. Metascape enrichment analysis and GO and KEGG enrichment analysis were conducted for differential expressed genes (DEGs). "randomForest" package in R software was used to screen characteristic genes of RA under random forest (RF) algorithm, and artificial neural network model was constructed according to gene score. Top 4 genes (HubGene) were extracted for subsequent analysis. Single sample gene set enrichment analysis (ssGSEA) was used to calculate abundance of immune cells in samples and carry out a series of correlation analysis. Results: Top 15 genes were selected as characteristic genes of RA through artificial neural network model: STAT1, RUNX3, AR, CDH11, LMO4, TIMP1, PLXNC1, CAP2, PRKAA2, VDR, SPP1, HCK, EPHB2, KCNAB1, ITGB7. STAT1, RUNX3 and CDH11 were up-regulated in RA synovial tissue, while AR was down-regulated in RA synovial tissue. Immune cell infiltration results showed that RA had the most significant correlation with activated CD4 T cells. Number of immune cells significantly related to RUNX3 was the largest. RUNX3 was significant positive correlated with activated B cells, activated CD4 T cells, activated CD8 T cells, central memory CD4+T cells, effector memory CD8 T cells, regulatory T cells, γδT cells and macrophages, while significant negative correlated with NK cells. Conclusion: Fifteen characteristic genes related to RA are identified through artificial neural network, among which STAT1, RUNX3, AR and CDH11 are top 4 genes. It emphasizes activation of CD4 T cells, regulatory T cells, γδT cells, macrophages, NK cells, activated B cells and other immune cells are important in pathogenesis of RA, providing new insights for diagnosis of RA and study of molecular mechanism of immune cells. [ABSTRACT FROM AUTHOR]