Peng Peng, Bai Li
Department of Microbiology and Immunology, School of Basic Medical Sciences, Dali University, Dali 671000, China.
Department of Microbiology and Immunology, School of Basic Medical Sciences, Dali University, Yunnan Key Laboratory for Biomedical Research and Developme nt of Insects, Dali University, Dali 671000, China. *Corresponding author, E-mail:
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2025 Apr;41(4):355-362.
Programmed death 1 (PD-1) and its ligand (PD-L1) serve as crucial targets in cancer immunotherapy, and their inhibitors have significantly improved the prognosis of many patients with malignant tumors. However, the issues of drug resistance and limited overall response rate associated with monotherapy remain prevalent. As a new generation of immune checkpoints, lymphocyte activation gene 3 (LAG-3) synergistically enhances the suppression of T cells alongside PD-1 in various cancers. Combining the blockade of both PD-1 and LAG-3 yields stronger anti-tumor immune effects compared to blocking either target alone, thereby reversing the immunosuppressive state of the tumor microenvironment and reducing the occurrence of resistance. This review covers the structural characteristics of LAG-3 and unveils its specific interactions with PD-1 across multiple cancers, providing a novel reference for overcoming the limitations of single-agent therapy.
程序性死亡蛋白1（PD-1）及其配体（PD-L1）是癌症免疫治疗的关键靶点，其抑制剂显著改善了许多恶性肿瘤患者的预后。然而，与单药治疗相关的耐药性和总体缓解率有限的问题仍然普遍存在。作为新一代免疫检查点，淋巴细胞激活基因3（LAG-3）在多种癌症中与PD-1协同增强对T细胞的抑制作用。与单独阻断任一靶点相比，联合阻断PD-1和LAG-3产生更强的抗肿瘤免疫效应，从而逆转肿瘤微环境的免疫抑制状态并减少耐药性的发生。本综述涵盖了LAG-3的结构特征，并揭示了其在多种癌症中与PD-1的具体相互作用，为克服单药治疗的局限性提供了新的参考。
