Exosome-Derived Cargos in Immune Microenvironment in Esophageal Carcinoma: A Mini-Review.

Yakun Zhang, Xiaoyan Sun, Yan Guan, Ying Sun
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Abstract

Esophageal carcinoma, a lethal malignancy with limited treatment options and poor prognosis, necessitates understanding its underlying mechanisms and identifying novel therapeutic targets. Recent studies have highlighted the critical role of the immune microenvironment in esophageal carcinoma, particularly the interplay between tumor cells and immune cells mediated by exosomes and their cargos. Exosomes, small extracellular vesicles secreted by various cells, including tumor cells, facilitate intercellular communication by transferring bioactive molecules such as proteins, nucleic acids, and lipids to recipient cells. In the context of esophageal carcinoma, tumor-derived exosomes have been shown to play a significant role in shaping the immune microenvironment. In esophageal carcinoma, exosomal cargos have been found to modulate immune cell function and impact tumor progression. These cargos can carry immune inhibitory molecules, such as programmed death-ligand 1 (PD-L1), to suppress T-cell activity and promote immune evasion by tumor cells. Furthermore, exosomal cargos can activate antigen- presenting cells, enhancing their ability to present tumor-specific antigens to T cells and thereby promoting anti-tumor immune responses. Additionally, the cargos of exosomes have been implicated in the induction of immune regulatory T cells (Tregs) and myeloid-derived suppressor cells (MDSCs) within the esophageal carcinoma microenvironment. These immunosuppressive effectors inhibit the activity of T cells, contributing to tumor immune evasion and resistance to immune therapies. In summary, exosomes and their cargo play a crucial role in the immune microenvironment of esophageal carcinoma. Understanding the mechanisms by which exosomal cargos regulate immune cell function and tumor progression may reveal novel therapeutic targets for this devastating disease.

食管癌免疫微环境中的外泌体衍生碳水化合物:微型综述
食管癌是一种致命的恶性肿瘤,治疗方案有限且预后不良,因此有必要了解其潜在机制并确定新的治疗靶点。最近的研究强调了免疫微环境在食管癌中的关键作用,特别是由外泌体及其载体介导的肿瘤细胞与免疫细胞之间的相互作用。外泌体是由包括肿瘤细胞在内的各种细胞分泌的小细胞外囊泡,通过将蛋白质、核酸和脂质等生物活性分子转移到受体细胞,促进细胞间的交流。就食管癌而言,肿瘤衍生的外泌体已被证明在塑造免疫微环境方面发挥了重要作用。在食管癌中,已发现外泌体载体可调节免疫细胞功能并影响肿瘤进展。这些载体可携带免疫抑制分子,如程序性死亡配体 1 (PD-L1),从而抑制 T 细胞活性,促进肿瘤细胞逃避免疫。此外,外泌体载体还能激活抗原呈递细胞,增强它们向 T 细胞呈递肿瘤特异性抗原的能力,从而促进抗肿瘤免疫反应。此外,外泌体载体还与食管癌微环境中免疫调节 T 细胞(Tregs)和髓源抑制细胞(MDSCs)的诱导有关。这些免疫抑制效应因子抑制了 T 细胞的活性,导致肿瘤免疫逃避和对免疫疗法的抵抗。总之,外泌体及其载体在食管癌的免疫微环境中起着至关重要的作用。了解外泌体载体调节免疫细胞功能和肿瘤进展的机制,可能会发现治疗这种毁灭性疾病的新靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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