Fig. 5: STAT3 pharmacological targeting reduces lung damage and immune dysfunctions in vFLIP mice.
From: Fatal cytokine release syndrome by an aberrant FLIP/STAT3 axis

A Analysis of cytokines levels in serum of vFLIP mice before treatment (T0) or at the end of treatment (untreated, n = 9; silibinin, n = 9; baricitinib, n = 9). B Lymphocytes (B cells: B220+ cells; T cells: CD3+ cells) and macrophages (F4/80+ cells) quantification in spleens of untreated (n = 14), silibinin (n = 8), and baricitinib (n = 16) vFLIP mice by H&E staining. Scale bar, 200 μm. C Pathological score of lungs of untreated (n = 14), silibinin (n = 8), and baricitinib (n = 16) vFLIP mice by H&E staining. Scale bar, 200 μm. D tSNE representation of scRNA-seq from untreated (4662) mice and treated with silibinin (3414) and baricitinib (4177) colored according to cell type. Stacked bar plots representing cell-type proportions across conditions. E Bar plot representing the up- and downregulated (adjusted p-value <0.05) hallmark gene sets obtained in the bulk-like analysis of treated compared to untreated vFLIP chimera cells obtained through GSEA analysis. F Violin plots showing the expression of genes involved in inflammatory response, JAK-STAT3 signaling pathway, and interferon response in the lung of vFLIP chimera mice (*p < 0.05, **p < 0.01, ***p < 0.001). Data are reported as mean ± S.E.M. *p ≤ 0.05, **p ≤ 0.01, and ***p ≤ 0.001 by Student’s t-test, Mann–Whitney test.