Modulating T cell immune checkpoints and inhibiting chemokine receptors on myeloid-derived suppressor cells can change the highly suppressive tumor immune microenvironment in PDAC and lead to long-lasting complete responses in a mouse model. These findings offer a testable clinical treatment strategy for PDAC in humans.
Modulation of T cell immune checkpoints combined with inhibition of chemokine receptors on myeloid-derived suppressor cells can reprogram the highly suppressive tumor immune microenvironment of pancreatic ductal adenocarcinoma (PDAC), and generates durable complete responses in a PDAC mouse model. These results provide a testable clinical regimen for human PDAC.
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