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. 2020 May 13;10:7907. doi: 10.1038/s41598-020-64431-4

Figure 2.

Figure 2

Transcriptome profiles distinguish RA- from OA-synovial tissues (ST) and reveal involvement of innate and adaptive immunity in RA pathogenesis. (A) Hierarchical clustering (Euclidean distance, average linkage) with 2019 differentially expressed probe-sets (rows), which were identified by pair-wise comparisons between RA (n = 10) and OA (n = 10) synovial tissue transcriptomes, separate RA from OA samples (columns). Signals were log-transformed and z-normalized for each probe set to display relative intensities as indicated by the scale bar. Principal component analysis (PCA) was performed for the 20 samples based on the differentially expressed genes (B). Based on this PCA, a synchronized representation of the 2019 probe-sets is displayed in (C). The first 3 principal components, PC1, PC2, and PC3, reflect 42%, 9% and 7% of variance, respectively. Samples from RA patients were coloured in red, those from OA in green (A and B). Probe-sets highest in RA-ST (n = 1010) are red and those highest in OA-ST (n = 1009) are blue (A and C). Gene set enrichment analysis (GSEA) of the 2019 differentially expressed probe-sets identified particular KEGG pathways for RA-ST and OA-ST, which suggest different pathomechanisms in these two diseases. The KEGG pathways presented here with enrichment plots and heatmaps of gene-sets accentuated the role of innate immunity, cytokines, B-, T- and NK-cells in RA pathogenesis (D–H) and tissue damage without substantial activation of the immune system in OA (I–M).