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Fig. 4 | Journal of Experimental & Clinical Cancer Research

Fig. 4

From: Inhibition of choline metabolism in an angioimmunoblastic T-cell lymphoma preclinical model reveals a new metabolic vulnerability as possible target for treatment

Fig. 4

ERK-MAPK and the PI3K-AKT-mTOR pathways are induced in human AITL CD4 + PD1 + Tfh-like cells. A Schematic presentation of the pathway producing PC and its further conversion into PA (phosphatidic acid), which activates ERK-MAPK and PI3K-Akt pathways. B Expression levels of PDL1 and PDL2 for the different T-cell populations (AITL patient Tfh cells (n = 8), healthy Tfh cells (n = 12), central memory T cells (Tcm) (n = 6), effector memory T cells (Tem) (n = 6), naive T cells (Tn) (n = 6), regulatory T cells (T reg) (n = 13) and stem memory T cell (Tscm) (n = 6) (mean ± SD; *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001). C Heatmap for GSEA data of 22 genes implicated in the ERK-MAPK target gene signature for AITL patient Tfh cells (n = 8), healthy Tfh cells (n = 12), central memory T cells (Tcm) (n = 6), effector memory T cells (Tem) (n = 6), naive T cells (Tn) (n = 6), regulatory T cells (T reg) (n = 13) and stem memory T cell (Tscm) (n = 6). Bubble representations for sample enrichment score (SES) of the ERK-MAPK target gene signature is shown (Bubbles size and numbers represents SES), p-value = 1.11e-024). D Heatmap for GSEA data of gene signature implicated in PI3K-Akt-mTOR signaling for the same T-cell subpopulations mentioned in (C). Bubble representations for sample enrichment score (SES) of the PI3K-Akt-mTOR signaling gene signature is shown (Bubbles size and numbers represents SES), p-value = 3.31e-017)

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