
Immune checkpoint inhibitor (ICI) therapy in non-small cell lung cancer (NSCLC) patients leads to reduced pro-inflammatory cytokines and a distinctive reduction in the expression of the anti-apoptotic molecule c-FLIP in monocytic myeloid-derived suppressor cells. This alteration mitigates systemic inflammation and impairs MDSC-dependent immunosuppression, suggesting the potential of ICI therapy in reshaping the immunological landscape in NSCLC.
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