Abstract
Immunologic checkpoint blockade (ICB) is a novel approach to reverse cancer immunosuppression. Various studies observed the role of CXCR2 in tumour aggressiveness, resistance and immune-suppression. CXCR2 signaling is known to recruit myeloid derived suppressor cells (MDSCs) to tumor microenvironment where MDSCs oppose the cytotoxic T-cell-mediated antitumor effect and suppress ICB efficacy. CXCR2 inhibition was found to augment programed cell death-1 (PD-1) inhibition in pancreatic cancer. CXCR2 inhibition has been proposed as an attractive anti-tumor treatment not only to enhance immunotherapy, but also to intensify the cytotoxicity of chemotherapeutic drugs.
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