Cancer is the second cause of mortality in the world after cardiovascular disease. Various studies attribute the emergence of therapeutic resistance in tumors to the presence of cancer stem cells or cancer-initiating cells (CSC/CIC). These relatively rare cells because of their typical stemness features, are responsible for tumor cell progression and recurrence. Moreover, CSCs have immunomodulatory capabilities and through orchestrating, some immunological profiles can stay safe from host anticancer immunity, and provide immunotherapy resistance in cancer patients. Many studies have shown that CSCs by producing immune system inhibitory factors and interacting with immune checkpoint molecules like CD47, PDL-1, CTLA4, Tim3, and LAG3, are able to communicate with tumor microenvironment (TME) components and protect cancer cells from immune clearance. In this review, we summarize the CSCs immunological mechanisms and comprehensively discuss interactions between these cells and factors that are present in the TME to repress immune system responses and enhance tumor survival. Therefore, it seems that further studies on this topic will open new doors to improve the therapeutic approaches of malignant cancers.

癌症是继心血管疾病之后世界上第二大死亡原因。各种研究将肿瘤中治疗抗性的出现归因于癌症干细胞或癌症起始细胞（CSC / CIC）的存在。这些相对稀有的细胞由于其典型的干性特征，导致肿瘤细胞的进展和复发。此外，CSC具有免疫调节功能，通过协调，某些免疫学特征可以保持对宿主抗癌免疫的安全性，并为癌症患者提供免疫治疗抗性。许多研究表明，CSC通过产生免疫系统抑制因子并与CD47，PDL-1，CTLA4，Tim3和LAG3等免疫检查点分子相互作用，能够与肿瘤微环境（TME）组分进行通讯并保护癌细胞免受免疫清除。在这篇综述中，我们总结了CSCs的免疫学机制，并全面讨论了这些细胞与TME中存在的相互作用之间的相互作用，以抑制免疫系统反应并增强肿瘤存活率。因此，似乎对该主题的进一步研究将为改善恶性肿瘤的治疗方法打开新的大门。