癌症干细胞的免疫逃避导致了肿瘤的发生和免疫治疗的失败

S. Chakraborty, S. Mukherjee, Udit Basak, Subhadip Pati, A. Dutta, Saikat Dutta, Subhanki Dhar, Tania Sarkar, A. Guin, G. Sa, T. Das
{"title":"癌症干细胞的免疫逃避导致了肿瘤的发生和免疫治疗的失败","authors":"S. Chakraborty, S. Mukherjee, Udit Basak, Subhadip Pati, A. Dutta, Saikat Dutta, Subhanki Dhar, Tania Sarkar, A. Guin, G. Sa, T. Das","doi":"10.37349/ei.2023.00108","DOIUrl":null,"url":null,"abstract":"Cancer stem cells (CSCs) are a small subpopulation of cells that drive the formation and progression of tumors. However, during tumor initiation, how CSCs communicate with neighbouring immune cells to overcome the powerful immune surveillance barrier in order to form, spread, and maintain the tumor, remains poorly understood. It is, therefore, absolutely necessary to understand how a small number of tumor-initiating cells (TICs) survive immune attack during (a) the “elimination phase” of “tumor immune-editing”, (b) the establishment of regional or distant tumor after metastasis, and (c) recurrence after therapy. Mounting evidence suggests that CSCs suppress the immune system through a variety of distinct mechanisms that ensure the survival of not only CSCs but also non-stem cancer cells (NSCCs), which eventually form the tumor mass. In this review article, the mechanisms via which CSCs change the immune landscape of the tissue of origin, which contains macrophages, dendritic cells (DCs), myeloid-derived suppressor cells (MDSCs), natural killer (NK) cells, and tumor-infiltrating lymphocytes, in favour of tumorigenesis were discussed. The failure of cancer immunotherapy might also be explained by such interaction between CSCs and immune cells. This review will shed light on the critical role of CSCs in tumor immune evasion and emphasize the importance of CSC-targeted immunotherapy as a cutting-edge technique for battling cancer by restricting communication between immune cells and CSCs.","PeriodicalId":93552,"journal":{"name":"Exploration of immunology","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2023-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":"{\"title\":\"Immune evasion by cancer stem cells ensures tumor initiation and failure of immunotherapy\",\"authors\":\"S. Chakraborty, S. Mukherjee, Udit Basak, Subhadip Pati, A. Dutta, Saikat Dutta, Subhanki Dhar, Tania Sarkar, A. Guin, G. Sa, T. Das\",\"doi\":\"10.37349/ei.2023.00108\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Cancer stem cells (CSCs) are a small subpopulation of cells that drive the formation and progression of tumors. However, during tumor initiation, how CSCs communicate with neighbouring immune cells to overcome the powerful immune surveillance barrier in order to form, spread, and maintain the tumor, remains poorly understood. It is, therefore, absolutely necessary to understand how a small number of tumor-initiating cells (TICs) survive immune attack during (a) the “elimination phase” of “tumor immune-editing”, (b) the establishment of regional or distant tumor after metastasis, and (c) recurrence after therapy. Mounting evidence suggests that CSCs suppress the immune system through a variety of distinct mechanisms that ensure the survival of not only CSCs but also non-stem cancer cells (NSCCs), which eventually form the tumor mass. In this review article, the mechanisms via which CSCs change the immune landscape of the tissue of origin, which contains macrophages, dendritic cells (DCs), myeloid-derived suppressor cells (MDSCs), natural killer (NK) cells, and tumor-infiltrating lymphocytes, in favour of tumorigenesis were discussed. The failure of cancer immunotherapy might also be explained by such interaction between CSCs and immune cells. This review will shed light on the critical role of CSCs in tumor immune evasion and emphasize the importance of CSC-targeted immunotherapy as a cutting-edge technique for battling cancer by restricting communication between immune cells and CSCs.\",\"PeriodicalId\":93552,\"journal\":{\"name\":\"Exploration of immunology\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2023-08-31\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"1\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Exploration of immunology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.37349/ei.2023.00108\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Exploration of immunology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.37349/ei.2023.00108","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 1

摘要

癌症干细胞(CSCs)是驱动肿瘤形成和发展的一个小的细胞亚群。然而,在肿瘤发生过程中,CSC如何与邻近的免疫细胞通信,以克服强大的免疫监视屏障,从而形成、传播和维持肿瘤,目前尚不清楚。因此,绝对有必要了解在(a)“肿瘤免疫编辑”的“消除阶段”,(b)转移后建立区域或远处肿瘤,以及(c)治疗后复发期间,少数肿瘤起始细胞(TIC)是如何在免疫攻击中存活的。越来越多的证据表明,CSC通过多种不同的机制抑制免疫系统,这些机制不仅确保CSC的存活,而且确保最终形成肿瘤团的非系统癌症细胞(NSCCs)的存活,讨论了骨髓来源的抑制细胞(MDSCs)、自然杀伤细胞(NK)和肿瘤浸润淋巴细胞有利于肿瘤发生。癌症免疫疗法的失败也可以通过CSC和免疫细胞之间的这种相互作用来解释。这篇综述将阐明CSC在肿瘤免疫逃避中的关键作用,并强调CSC靶向免疫疗法作为通过限制免疫细胞和CSC之间的交流来对抗癌症的尖端技术的重要性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
Immune evasion by cancer stem cells ensures tumor initiation and failure of immunotherapy
Cancer stem cells (CSCs) are a small subpopulation of cells that drive the formation and progression of tumors. However, during tumor initiation, how CSCs communicate with neighbouring immune cells to overcome the powerful immune surveillance barrier in order to form, spread, and maintain the tumor, remains poorly understood. It is, therefore, absolutely necessary to understand how a small number of tumor-initiating cells (TICs) survive immune attack during (a) the “elimination phase” of “tumor immune-editing”, (b) the establishment of regional or distant tumor after metastasis, and (c) recurrence after therapy. Mounting evidence suggests that CSCs suppress the immune system through a variety of distinct mechanisms that ensure the survival of not only CSCs but also non-stem cancer cells (NSCCs), which eventually form the tumor mass. In this review article, the mechanisms via which CSCs change the immune landscape of the tissue of origin, which contains macrophages, dendritic cells (DCs), myeloid-derived suppressor cells (MDSCs), natural killer (NK) cells, and tumor-infiltrating lymphocytes, in favour of tumorigenesis were discussed. The failure of cancer immunotherapy might also be explained by such interaction between CSCs and immune cells. This review will shed light on the critical role of CSCs in tumor immune evasion and emphasize the importance of CSC-targeted immunotherapy as a cutting-edge technique for battling cancer by restricting communication between immune cells and CSCs.
求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
CiteScore
1.00
自引率
0.00%
发文量
0
期刊最新文献
Exploring the impact of immune response on tumor heterogeneity through mathematical modeling Recent advances in the study of the structure and function of the epididymis The immune response of nano carbon-based photic-driving vaccines to severe acute respiratory syndrome coronavirus 2 Targeted treatments for immune dysregulation in inborn errors of immunity Physical activity, immune system and hypertension: reflections and challenges for future pandemics based on learning from coronavirus disease 2019
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1