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Fig. 8 | Journal of Translational Medicine

Fig. 8

From: Cancer stem cell-derived CHI3L1 activates the MAF/CTLA4 signaling pathway to promote immune escape in triple-negative breast cancer

Fig. 8

Schematic illustration of the molecular mechanism by which TN-BCSC-derived CHI3L1 promotes immune escape of TNBC via the MAF/CTLA4 axis. TNBC mainly contains 8 cell subsets, among which TN-BCSCs exist in the epithelial cell subgroup. As a characteristic gene expressed in TN-BCSCs, CHI3L1 is related to TNBC cell stemness. It upregulates the expression of CTLA4 in T cells through MAF, thereby inhibiting the cytotoxicity of CD8+ T cells and producing immunosuppression. CTLA4+ T cells promote the stemness phenotype of TNBC cells by secreting S100A4 through positive feedback

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Journal of Translational Medicine

ISSN: 1479-5876

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