肿瘤细胞治疗研究
英文原题：Cancer cell-derived extracellular vesicles: a potential target for overcoming tumor immunotherapy resistance and immune evasion strategies.
Cancer cell-derived extracellular vesicles: a potential target for overcoming tumor immunotherapy resistance and immune evasion strategies.
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细胞外囊泡（EVs），包括外泌体和微囊泡，通过介导癌细胞与其微环境之间的通讯，在癌症进展中发挥关键作用。癌细胞来源的EVs通过携带生物活性物质，如蛋白质、RNAs、DNA片段和脂质，促进肿瘤生长、转移和免疫逃逸，而免疫治疗旨在增强针对癌症的免疫反应；然而，耐药性仍然是一个重大挑战。癌细胞来源的EVs通过递送免疫抑制分子导致这种耐药性，这些分子损害T细胞活化，促进调节性T细胞（Tregs）的扩增，并降低自然杀伤（NK）细胞的细胞毒性，从而使癌细胞能够逃避免疫监视。
此外，癌细胞来源的EVs可以携带免疫检查点蛋白，如程序性死亡配体1（PD-L1），其与T细胞上的程序性死亡-1（PD-1）受体结合，导致T细胞耗竭和抗肿瘤活性降低。这一机制反映了癌细胞如何直接逃避免疫检测，并导致对免疫检查点阻断疗法（如抗PD-1或抗PD-L1抗体）的整体耐药性。通过递送这些免疫调节分子，EVs不仅促进局部免疫抑制，还创造一个对有效抗癌免疫不太有利的全身环境。
因此，了解EVs在免疫治疗耐药性中的作用对于开发针对性策略以抵消其影响并最终改善治疗结果至关重要。在此，我们鼓励研究人员更多关注癌细胞来源的EV在克服免疫治疗耐药中的作用，因为这类努力可能是未来解决免疫治疗耐药最有前景的途径之一。
Extracellular vesicles (EVs), including exosomes and microvesicles, play crucial roles in cancer progression by mediating the communication between cancer cells and their microenvironment. Cancer cell-derived EVs promote tumor growth, metastasis, and immune evasion by carrying bioactive materials, such as proteins, RNAs, DNA fragments, and lipids but, immunotherapy aims to enhance the immune response against cancer; however, resistance remains a major challenge.
Cancer cell-derived EVs contribute to this resistance by delivering immunosuppressive molecules that impair T cell activation, promote the expansion of regulatory T cells (Tregs), and reduce natural killer (NK) cell cytotoxicity, thereby allowing cancer cells to evade immune surveillance.
Additionally, cancer cell-derived EVs can carry immune checkpoint proteins, such as Programmed Death-Ligand 1 (PD-L1), which bind to the Programmed Death-1 (PD-1) receptor on T cells, leading to T cell exhaustion and reduced anti-tumor activity.
This mechanism reflects how cancer cells directly evade immune detection and contributes to the overall resistance to immune checkpoint blockade therapies, such as anti-PD-1 or anti-PD-L1 antibodies. By delivering these immunomodulatory molecules, EVs not only contribute to local immune suppression but also create a systemic environment that is less favorable for effective anticancer immunity.
Therefore, understanding the role of EVs in the immunotherapy resistance is crucial for developing targeted strategies to counteract their effects and ultimately improve therapeutic outcomes.
Here we encourage researchers to pay more attention to the role of cancer cell-derived EVs in overcoming immunotherapeutic resistance, because such efforts may be one of the most promising approaches to address immunotherapy resistance in the future.
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