结直肠癌 (CRC) 起源于结肠内壁息肉，是最常见的癌症类型之一。随着单细胞测序技术的日益普及，研究人员通过在单细胞水平上详细分析结直肠癌的表达及其与肿瘤微环境（TME）的相互作用，能够更好地了解结直肠癌的免疫状况。由于肿瘤-免疫细胞相互作用在结直肠癌的进展和治疗反应中发挥着关键作用，因此 T 细胞等抑制因子的释放对于识别和破坏癌细胞非常重要。这些信息对于确定治愈的免疫治疗靶点和监测治疗反应至关重要。因此，本综述对调节 CRC TME 的关键免疫原性药物进行了基于单细胞研究的全面概述。肿瘤相关巨噬细胞可以通过释放抑制其他免疫细胞功能的因子来促进肿瘤生长和对治疗的抵抗力。此外，结直肠癌细胞可以表达程序性细胞死亡蛋白1及其配体，也可以抑制T细胞功能。研究人员发现，某些类型的免疫细胞，特别是 T 细胞、自然杀伤细胞和树突状细胞，可以对结直肠癌患者的预后产生积极影响。免疫检查点抑制剂和 CAR-T 疗法等治疗有助于释放癌细胞的抑制信号，使免疫细胞更有效地发挥作用。© 2023。作者获得 Springer Science Business Media, LLC 的独家许可，施普林格自然的一部分。

Colorectal cancer (CRC) originates from the polyps lining the colon and is among the most common types of cancer. With the increasing popularity of single-cell sequencing technologies, researchers have been able to better understand the immune landscape of colorectal cancer, by analyzing their expression and interactions in detail with the tumor microenvironment (TME) at single-cell level. Since the tumor-immune cell interactions play a critical part in the advancement as well as treatment response in colorectal cancer, the release of inhibitory factors such as T cells are important for recognizing and destroying cancer cells. Such information is vital to identify immunotherapeutic targets for cure and monitoring response to treatments. Therefore, a comprehensive single-cell studies-based overview of key immunogenic agents regulating the TME of CRC is provided in this review. Tumor-associated macrophages can promote tumor growth and resistance to treatment by releasing factors that inhibit the function of other immune cells. Additionally, colorectal cancer cells can express programmed cell death protein 1 and its ligand, which can also inhibit T-cell function. Researchers have found that certain types of immune cells, prominently T cells, natural killer, and dendritic cells, can have a positive impact on the prognosis of colorectal cancer patients. Treatments like immune checkpoint inhibitors and CAR-T therapies that help to release the inhibitory signals from the cancer cells allow the immune cells to function more effectively.© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.