同时抑制 PD-1 和 LAG-3：免疫治疗的未来？

Immunotherapy has improved the prognosis of many cancers, yet a large number of patients have demonstrated resistance to current immune checkpoint inhibitors. LAG-3 is an immune checkpoint expressed on tumor-infiltrating lymphocytes CD4 + and CD8 + , Tregs and other immune cells. Coexpression of PD-1 and LAG-3 in solid or hematological cancers is generally associated with a poor prognosis and may be responsible for immunotherapy resistance. Dual inhibition therapy in the RELATIVITY-047 trial significantly improved progression-free survival in metastatic melanoma. This article discusses the presence of a possible synergistic interaction between LAG-3 and PD-1 in the tumor microenvironment and the utility of targeting both immune checkpoint inhibitors as an effective way to bypass resistance and increase treatment efficacy.

Immunotherapy has increased survival rates for many cancer types; however, a large number of individuals experience resistance to this therapy and poor outcomes. Among the immune molecules expressed on immune cells and tumor cells, LAG-3 can favor tumor escape and progression. The coexpression of multiple immune molecules such as PD-1 and LAG-3 in multiple cancers is generally associated with a worse prognosis and might be contributing to immunotherapy failure.

Dual inhibition therapy, targeting both PD-1 and LAG-3, in the RELATIVITY-047 study has shown great antitumor activity and improved survival in metastatic melanoma. This report discusses a possible synergistic interaction between LAG-3 and PD-1 within the tumor and the utility of targeting both molecules as a way to overcome resistance and improve treatment efficacy.