生物信息学分析方法探讨类风湿关节炎患者滑膜病变中的免疫细胞浸润

Objective To explore the immune infiltration cells in rheumatoid arthritis (RA) synovial lesions, and to provide new research directions and therapeutic targets for the pathogenesis and treatment of RA. Methods The three gene expression data sets GSE77298, GSE55457 and GSE1919 were downloaded from gene expression omnibus (GEO) (http://www.ncbi.nlm.nih.gov/geo), and the data were merged with Perl. The "limma" package was used to adjust batch differences. In R, "CIBERSORT" software was used to obtain the expression matrix of 22 kinds of immune cells corresponding to RA synovial tissue samples and normal synovial tissue samples were analyzed with the three packages of "e1071", "parallel" and "preprocessCore". Perl was used to screen samples with P<0.05 in the immune cell matrix. R's "barplot" function was analyzed by the percentage of 22 immune cells in samples with P<0.05. The "pheatmap" package of R was used to visualize heatmaps, and "corrplot" package was used to draw correlation heatmaps. The "vioplot" package of R was used to draw violin plots of differences via the wilcox test. Results The results of immune cell infiltration analysis showed that in RA synovial tissue samples and normal synovial tissue samples at P<0.05, B cells naive and natural killer cells resting were under-expressed in RA synovial tissue, and plasma cells, mast cells resting, macrophages M1, B cells memory and T cells regulatory were highly expressed in RA synovial tissue. This study also found that in the same sample, the correlation coefficient between natural killer cells resting and neutrophils (r=0.91) was the highest, indicating synergistic effect between the two. In the same sample, the correlation coefficient between macrophages M0 and plasma cells (r=-0.88) was the lowest, indicating antagonistic effect between the two. Conclusion The immune infiltrating cells in RA synovial lesions discovered in this study provide a certain theoretical basis and research direction for the research on the disease mechanism and treatment of RA.