Extended Data Fig. 3: Increased expression of genes in NF-κB and type-I IFN pathways in patient PBMCs.
From: A dominant autoinflammatory disease caused by non-cleavable variants of RIPK1
a, Visualization of expression of genes involved in NF-κB pathway (SOCS3, CD40, TLR2, IL1RN, IL6, CD38, TAP1, IL15, ICOS, CD83, TNF, IFNG, CXCL2, FCGRT, TNFSF10, ICAM1, IGHG1, TNFRSF1B, CCL3, IGHG4 and TREM1) (coloured single cells) on UMAP plot projecting PBMCs from patient P1 (n = 7,936 cells) and an age- and sex-matched unaffected control (n = 10,992 cells). b, Visualization of expression of genes involved in type-I IFN signalling pathway (IFI6, IFI30, OAS1, GBP1, IFI27, ISG15, OAS2, SOCS1, IFI44, IRF7, OAS3, LY6E, IFI44L, MX1, OASL, RSAD2, IFIT3, HERC5, USP18, IFIT2, HERC6 and EPSTI1) (coloured single cells) on UMAP plot projecting PBMCs from patient P1 (n = 7,936 cells) and an age- and sex-matched unaffected control (n = 10,992 cells). The PBMCs from P1 in a and b were obtained during a fever episode.
