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. 2024 Oct 3;15:8571. doi: 10.1038/s41467-024-52826-0

Fig. 7. SAHA treatment remodels the tumor microenvironment of PTCL-NOSSmarcb1 and reduces the exhaustion phenotype in vivo.

Fig. 7

A Left: UMAP visualization of the integrated single-cell transcriptomes from control (WT), untreated, and SAHA-treated PTCL spleens (each n = 2 samples; 11,090 cells in total), Middle: relative contribution of different cellular compartments in the three sample groups; Right: pie charts showing the ratio between B-cells and myeloid cells in the three sample groups. B Expanded view of the T/NK cell compartment with a more detailed cell type annotation based on the dot plot shown in (C). D Proportions of distinct T/NK cell type subsets in the three sample groups. CM central memory T-cell, EM effector memory T-cell, Tex terminally exhausted T-cell, N/A unassigned cells. E Dot plot showing average expression levels (avg. exp.) and proportions of cells (pct. exp.) expressing exhaustion or cytotoxic marker genes in T-, NK and NKT cells from control, PTCL and SAHA-treated samples. F Trajectory analysis of Cd8+ T-cell clusters of untreated and SAHA-treated PTCL samples using STREAM99. Stream plot visualization of (from left to right): sample contribution (untreated = PTCL, black; treated = SAHA, gray), inferred phenotype and normalized expression (norm. exp.) of the cytotoxicity marker Gzmb and the exhaustion marker Pdcd1 (PD-1) along the pseudotime axis. Source data of D are provided as a Source Data file.