Fig 5. c-Maf signaling represents a key dysregulated pathway in proliferating HIV^pos GC-Tfh cells.

(A) shows log2-fold change (logFC) in the expression of selected DEGs in different cell signaling and GC-Tfh-associated immunological pathways in proliferating (CFSE^neg vs CFSE^pos) HIV^neg and HIV^pos GC-Tfh cells. Among these, are genes coding for transcription factors (E2F2) and coregulators (HOPX), enzymes (ADA) and key GC-Tfh genes (ICOS, IRF4, BCL6, MAF and mediators of its signaling pathway IL6R, STAT3, BATF). (B) table showing log2-fold change (logFC) values and statistical significance between proliferating HIV^pos versus HIV^neg GC-Tfh cells for each selected DEG in (A). To assess statistical significance between the logFC of proliferating HIV^pos versus HIV^neg GC-Tfh cells, data in (A) was analyzed using a double contrast. CFSE^neg values were baselined to CFSE^pos values and an HIV^pos versus HIV^neg contrast was performed to compare significance between (CFSE^neg vs CFSE^pos) HIV^pos and (CFSE^neg vs CFSE^pos) HIV^neg cells. (C-D) Venn diagram analysis of proliferating (CFSE^neg vs CFSE^pos) HIV^neg and HIV^pos GC-Tfh cells. Diagrams show the numbers of unique and common statistically significant DEGs in the indicated GC-Tfh populations. (C) shows Venn diagram analysis of upregulated DEGs (represented in purple) and (D) shows Venn diagram analysis of downregulated DEGs (represented in green) in HIV^neg and HIV^pos cells. (B-D) Analysis was performed based on nominal p-value p<0.05.