Fig. 6: Distribution of TH1, TH17, and immune activation-associated genes across cell clusters and time points. | Nature Communications

Fig. 6: Distribution of TH1, TH17, and immune activation-associated genes across cell clusters and time points.

From: Concurrent TB and HIV therapies control TB reactivation during co-infection but not chronic immune activation

Fig. 6: Distribution of TH1, TH17, and immune activation-associated genes across cell clusters and time points.

Violin plots displaying the distributions of 42 genes across cell clusters (color-coded) when comparing time points (wk 5, wk 11, wk 13 and Necropsy). These genes were associated with A TH1 (IFNG, IFNGR1, IFNGR2, TBX21, STAT1, TNFAIP2, TNFAIP3, TNFAIP8, TNFAIP8L1, TNFAIP8L3, IL2, IL2RA, and BHLHE40), B TH17 (IL20, IL20RA, IL20RB, IL21, IL21R, IL22, IL22RA1, IL22RA2, IL23A, IL23R, RORA, and STAT3), and C immune activation (IDO-1, IRF4, CD38, CD69, LAG3, ICOS, CTLA4, IL13, CXCL10, CXCR1, CXCL12, CXCL13, IL27, KLRD1, IL6, MMP9, and FCGR1A). Wilcoxon test of the distributions of differential gene expression (average log2 fold changes) between time points per cluster for D TH1, E TH17, and F Immune activation modules. In these analyses, enriched terms were defined as those with an FDR (Benjamini-Hochberg) corrected p value < 0.05 and a Storey’s q value < 0.05. All enrichment analyses were performed using the Bioconductor package clusterProfiler. A total of 24 samples were analyzed (six RMs x four time points = 24 samples in total).

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