Fig. 8: Distinct TGFβ level/activity contributes to different osteoclastic activity in RA and SLE patients. | Nature Communications

Fig. 8: Distinct TGFβ level/activity contributes to different osteoclastic activity in RA and SLE patients.

From: TGFβ reprograms TNF stimulation of macrophages towards a non-canonical pathway driving inflammatory osteoclastogenesis

Fig. 8

a Volcano plot of microarray analysis of the mRNA expression in the PBMCs isolated from SLE and RA patients. Blue dots: DEGs are more highly expressed in SLE PBMCs. Red dots: DEGs are more highly expressed in RA PBMCs. b, c Pathway analysis of the enriched DEGs in SLE (b) and RA (c). Note: c the upper TGFβ signaling Pathway ID is hsa04350 and the lower TGF-β Signaling Pathway ID is WP366. d Heatmaps of mRNA expression of the genes involved in osteoclasts, TGFβ signaling, Type-I IFN response, and Chemokine genes in the SLE and RA PBMCs. Row z-scores of Normalized Signal Intensity were shown in the heatmaps. n = 82 for SLE patients and n = 84 for RA patients. e Gene set enrichment analysis of DEG set (osteoclast, TGFβ signaling, type-I IFN response, and chemokine) in SLE and RA PBMCs. f Scatter plot showing the significantly positive correlation between the osteoclast activity and TGFβ activity. g Normalized Signal Intensity of TGFB1, IFNB1, IRF1, IRF8, FOXM1, and MYBL2 in SLE and RA PBMCs obtained from microarray data. n = 82 for SLE patients and n = 84 for RA patients. g *p < 0.05, **p < 0.01 by Welch’s t test (two-sided). Source data are provided as a Source Data file.

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