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NKG2D 在肿瘤微环境中定义了肿瘤反应性效应 CD8 T 细胞。

NKG2D defines tumor-reacting effector CD8 T cells within tumor microenvironment.

机构信息

Institute of Natural Medicine, University of Toyama, Toyama, Japan.

Department of Immunology, Graduate School of Medicine and Pharmaceutical Sciences (Medicine), Toyama, Japan.

出版信息

Cancer Sci. 2021 Sep;112(9):3484-3490. doi: 10.1111/cas.15050. Epub 2021 Jul 28.

Abstract

For successful immunotherapy for cancer, it is important to understand the immunological status of tumor antigen-specific CD8 T cells in the tumor microenvironment during tumor progression. In this study, we monitored the behavior of B16OVA-Luc cells in mice immunized with a model tumor antigen ovalbumin (OVA). Using bioluminescence imaging, we identified the time series of OVA-specific CD8 T-cell responses during tumor progression: initial progression, immune control, and the escape phase. As a result of analyzing the status of tumor antigen-specific CD8 cells in those 3 different phases, we found that the expression of NKG2D defines tumor-reacting effector CD8 T cells. NKG2D may control the fate and TOX expression of tumor-reacting CD8 T cells, considering that NKG2D blockade in OVA-vaccinated mice delayed the growth of the B16OVA-Luc2 tumor and increased the presence of tumor-infiltrating OVA-specific CD8 T cells.

摘要

为了实现癌症免疫治疗的成功,了解肿瘤进展过程中肿瘤微环境中肿瘤抗原特异性 CD8 T 细胞的免疫状态非常重要。在这项研究中,我们监测了用模型肿瘤抗原卵清蛋白(OVA)免疫的小鼠中 B16OVA-Luc 细胞的行为。通过生物发光成像,我们确定了肿瘤进展过程中 OVA 特异性 CD8 T 细胞反应的时间序列:初始进展、免疫控制和逃逸阶段。通过分析这 3 个不同阶段中肿瘤抗原特异性 CD8 细胞的状态,我们发现 NKG2D 的表达定义了肿瘤反应性效应 CD8 T 细胞。考虑到 NKG2D 阻断可延迟 B16OVA-Luc2 肿瘤的生长并增加肿瘤浸润性 OVA 特异性 CD8 T 细胞的存在,NKG2D 可能控制着肿瘤反应性 CD8 T 细胞的命运和 TOX 表达。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e33/8409295/98439b78a762/CAS-112-3484-g001.jpg

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