Extended Data Fig. 10: SRS1 signatures across differing clinical contexts of infectious disease.

a–e, BrWB-CID contexts 2–7. a, Cycling neutrophil progenitor proportions following whole blood bulk transcriptomics deconvolution in 6 cohorts of infectious disease patients defined by infecting organism (n = 77 COVID-19 and n = 109 influenza, top), source of infection (n = 438 community acquired pneumonia and n = 229 fecal peritonitis, middle) and clinical syndrome (n = 77 adult acute respiratory distress syndrome (ARDS) and n = 106 pediatric septic shock, bottom). Boxplots denote minimum and maximum with whiskers and bottom quartile, median and upper quartile with the box. Two-sided Wilcoxon rank-sum test comparing SRS1 and non-SRS1 groups. b, Gene set enrichment analysis of scWB STAT3 gene expression programs (GEPs) (the union of all three GEPs, STAT3-union-GEP) in SRS1 upregulated genes for each of the 6 cohorts. c, IL1R2+ immature neutrophil proportions in COVID-19 whole blood scRNA-seq cohort (n = 8) after referencing mapping of dataset to scWB reference single cell atlas. d, Violin plots of scWB neutrophil STAT3 GEP expression in COVID-19 neutrophils as defined by scWB neutrophil states. Two-sided Wilcoxon rank-sum test comparing SRS1 and non-SRS1 groups. e, Violin plots of scWB neutrophil STAT3-union-GEP expression in all COVID-19 neutrophils. Two-sided Wilcoxon rank-sum test comparing SRS1 and non-SRS1 groups. SRS, sepsis response signature; Neu, neutrophil. *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001.