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MHC Ⅰ类分子缺陷与实体瘤及克服策略

MHC Class I Deficiency in Solid Tumors and Therapeutic Strategies to Overcome It.

机构信息

Faculty of Medicine, Health and Human Sciences, Macquarie University, Sydney, NSW 2109, Australia.

出版信息

Int J Mol Sci. 2021 Jun 23;22(13):6741. doi: 10.3390/ijms22136741.

DOI:10.3390/ijms22136741
PMID:34201655
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8268865/
Abstract

It is now well accepted that the immune system can control cancer growth. However, tumors escape immune-mediated control through multiple mechanisms and the downregulation or loss of major histocompatibility class (MHC)-I molecules is a common immune escape mechanism in many cancers. MHC-I molecules present antigenic peptides to cytotoxic T cells, and MHC-I loss can render tumor cells invisible to the immune system. In this review, we examine the dysregulation of MHC-I expression in cancer, explore the nature of MHC-I-bound antigenic peptides recognized by immune cells, and discuss therapeutic strategies that can be used to overcome MHC-I deficiency in solid tumors, with a focus on the role of natural killer (NK) cells and CD4 T cells.

摘要

现在人们普遍认为免疫系统可以控制癌症的生长。然而,肿瘤通过多种机制逃避免疫介导的控制,主要组织相容性复合体(MHC)-I 分子的下调或缺失是许多癌症中常见的免疫逃逸机制。MHC-I 分子向细胞毒性 T 细胞呈递抗原肽,而 MHC-I 的缺失会使肿瘤细胞对免疫系统不可见。在这篇综述中,我们研究了癌症中 MHC-I 表达的失调,探讨了免疫细胞识别的 MHC-I 结合抗原肽的性质,并讨论了可以用于克服实体瘤中 MHC-I 缺陷的治疗策略,重点讨论了自然杀伤(NK)细胞和 CD4 T 细胞的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7324/8268865/8063225eb829/ijms-22-06741-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7324/8268865/543a87c44448/ijms-22-06741-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7324/8268865/479e7756989e/ijms-22-06741-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7324/8268865/6f0b5c333611/ijms-22-06741-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7324/8268865/8063225eb829/ijms-22-06741-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7324/8268865/543a87c44448/ijms-22-06741-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7324/8268865/479e7756989e/ijms-22-06741-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7324/8268865/6f0b5c333611/ijms-22-06741-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7324/8268865/8063225eb829/ijms-22-06741-g004.jpg

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