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癌症免疫治疗中的淋巴细胞激活基因3：功能、预后生物标志物及治疗潜力

Lymphocyte-activation gene 3 in cancer immunotherapy: function, prognostic biomarker and therapeutic potentials.

作者信息

Ren Ke, Hamdy Hayam, Meyiah Abdo, Elkord Eyad

机构信息

Department of Biosciences and Bioinformatics, School of Science, Suzhou Municipal Key Lab in Biomedical Sciences and Translational Immunology, Xi'an Jiaotong-Liverpool University, Suzhou, Jiangsu, China.

Department of Forensic Medicine and Toxicology, Faculty of Veterinary Medicine, New Valley University, New Valley, Egypt.

出版信息

Front Immunol. 2024 Nov 26;15:1501613. doi: 10.3389/fimmu.2024.1501613. eCollection 2024.

DOI:10.3389/fimmu.2024.1501613
PMID:39660130
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11628531/
Abstract

Lymphocyte-activation gene 3 (LAG-3) has emerged as a key immune checkpoint regulating immune responses in the context of cancer. The inhibitory effect of LAG-3-expressing T cells contributes to suppressing anti-tumor immunity and promoting tumor progression. This review discusses the function of LAG-3 in immune suppression, its interactions with ligands, and its potential as a prognostic biomarker for cancers. We also explore therapeutic strategies targeting LAG-3, including monoclonal antibodies, small molecule inhibitors, and CAR T cells. This review summarizes the current preclinical and clinical studies on LAG-3, highlighting the potential of therapeutic regimens targeting LAG-3 to enhance antitumor immunity and improve patients' outcomes. Further studies are needed to fully elucidate the mechanism of action of LAG-3 and optimize its application in tumor therapy.

摘要

淋巴细胞激活基因3（LAG-3）已成为癌症背景下调节免疫反应的关键免疫检查点。表达LAG-3的T细胞的抑制作用有助于抑制抗肿瘤免疫并促进肿瘤进展。本综述讨论了LAG-3在免疫抑制中的功能、其与配体的相互作用及其作为癌症预后生物标志物的潜力。我们还探索了针对LAG-3的治疗策略，包括单克隆抗体、小分子抑制剂和嵌合抗原受体T细胞（CAR T细胞）。本综述总结了目前关于LAG-3的临床前和临床研究，强调了针对LAG-3的治疗方案增强抗肿瘤免疫力和改善患者预后的潜力。需要进一步研究以充分阐明LAG-3的作用机制并优化其在肿瘤治疗中的应用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb38/11628531/3d1568559c8b/fimmu-15-1501613-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb38/11628531/025fbdd31456/fimmu-15-1501613-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb38/11628531/accf7fca632a/fimmu-15-1501613-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb38/11628531/15d46c663999/fimmu-15-1501613-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb38/11628531/d3a86d2de97c/fimmu-15-1501613-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb38/11628531/3d1568559c8b/fimmu-15-1501613-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb38/11628531/025fbdd31456/fimmu-15-1501613-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb38/11628531/accf7fca632a/fimmu-15-1501613-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb38/11628531/15d46c663999/fimmu-15-1501613-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb38/11628531/d3a86d2de97c/fimmu-15-1501613-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb38/11628531/3d1568559c8b/fimmu-15-1501613-g005.jpg

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Signal Transduct Target Ther. 2024 Oct 18;9(1):291. doi: 10.1038/s41392-024-02000-1.
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Blockade of LAG-3 and PD-1 leads to co-expression of cytotoxic and exhaustion gene modules in CD8 T cells to promote antitumor immunity.阻断 LAG-3 和 PD-1 导致 CD8 T 细胞共表达细胞毒性和耗竭基因模块，以促进抗肿瘤免疫。
Cell. 2024 Aug 8;187(16):4373-4388.e15. doi: 10.1016/j.cell.2024.06.036.
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LAG-3 and PD-1 synergize on CD8 T cells to drive T cell exhaustion and hinder autocrine IFN-γ-dependent anti-tumor immunity.
LAG-3 和 PD-1 在 CD8 T 细胞上协同作用，导致 T 细胞耗竭，并阻碍自分泌 IFN-γ 依赖的抗肿瘤免疫。
Cell. 2024 Aug 8;187(16):4355-4372.e22. doi: 10.1016/j.cell.2024.07.016.
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LAG-3 sustains TOX expression and regulates the CD94/NKG2-Qa-1b axis to govern exhausted CD8 T cell NK receptor expression and cytotoxicity.LAG-3 维持 TOX 的表达，并调节 CD94/NKG2-Qa-1b 轴以控制耗竭的 CD8 T 细胞 NK 受体表达和细胞毒性。
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Anti-LAG-3 boosts CD8 T cell effector function.抗 LAG-3 增强 CD8 T 细胞效应功能。
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