Bidirectional crosstalk between epithelial-mesenchymal plasticity and IFN-induced PD-L1 expression promotes tumour progression.

Epithelial-mesenchymal transition (EMT) and immunoevasion through upregulation of programmed death-ligand 1 (PD-L1) are important drivers of cancer progression. While EMT has been proposed to facilitate PD-L1-mediated immunosuppression, molecular mechanisms of their interaction remain obscure. Here, we provide insight into these mechanisms by proposing a mathematical model that describes the crosstalk between EMT and interferon gamma (IFN)-induced PD-L1 expression.