The magnitude of the host immune response can be regulated by either stimulatory oas ba?adores or inhibitory immune checkpoint molecules.Receptor-ligand binding between inhibitory molecules is often exploited by tumours to suppress anti-tumour immune responses.Immune checkpoint inhibitors that block these inhibitory interactions can relieve T-cells from negative regulation, and have yielded remarkable activity in the clinic.
Despite this success, clinical data reveal that durable responses are limited to a minority of patients and malignancies, indicating the presence of underlying resistance mechanisms.Accumulating evidence suggests that tumour hypoxia, a pervasive feature of many solid cancers, is a critical yazhi design saree phenomenon involved in suppressing the anti-tumour immune response generated by checkpoint inhibitors.In this review, we discuss the mechanisms associated with hypoxia-mediate immunosuppression and focus on modulating tumour hypoxia as an approach to improve immunotherapy responsiveness.