Genetics Division, Department of Cell and Molecular Biology and Microbiology, Faculty of Science and Technology, University of Isfahan, Isfahan, Iran.
Medical Campus, Xi'an Jiaotong University, Xi'an, Shaanxi Province, China.
Cell Mol Life Sci. 2024 Feb 29;81(1):106. doi: 10.1007/s00018-023-05098-8.
Advances in cancer immunotherapy over the last decade have led to the development of several agents that affect immune checkpoints. Inhibitory receptors expressed on T cells that negatively regulate the immune response include cytotoxic T‑lymphocyte antigen 4 (CTLA4) and programmed cell death protein 1 (PD1), which have been studied more than similar receptors. Inhibition of these proteins and other immune checkpoints can stimulate the immune system to attack cancer cells, and prevent the tumor from escaping the immune response. However, the administration of anti-PD1 and anti-CTLA4 antibodies has been associated with adverse inflammatory responses similar to autoimmune diseases. The current review discussed the role of the NF-κB pathway as a tumor promoter, and how it can govern inflammatory responses and affect various immune checkpoints. More precise knowledge about the communication between immune checkpoints and NF-κB pathways could increase the effectiveness of immunotherapy and reduce the adverse effects of checkpoint inhibitor therapy.
过去十年中，癌症免疫疗法的进展促使了几种影响免疫检查点的药物的发展。表达在 T 细胞上的抑制性受体通过负向调节免疫反应，包括细胞毒性 T 淋巴细胞抗原 4（CTLA4）和程序性死亡蛋白 1（PD1），它们比类似的受体受到了更多的研究。抑制这些蛋白和其他免疫检查点可以刺激免疫系统攻击癌细胞，并防止肿瘤逃避免疫反应。然而，抗 PD1 和抗 CTLA4 抗体的给药与类似自身免疫性疾病的不良反应性炎症反应有关。本综述讨论了 NF-κB 途径作为肿瘤促进剂的作用，以及它如何控制炎症反应并影响各种免疫检查点。对免疫检查点和 NF-κB 途径之间的通讯有更精确的了解，可能会提高免疫疗法的有效性，并降低检查点抑制剂治疗的不良反应。
