CD81 通过阻断 CD274/PD-L1 的选择性自噬降解驱动放射抵抗性胶质母细胞瘤的免疫逃逸
CD81 drives immune evasion in radioresistant glioblastoma by blocking selective autophagic degradation of CD274/PD-L1.
CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
I 型干扰素信号调控胶质母细胞瘤肿瘤微环境中髓系细胞与 T 细胞的交互作用
英文原题：Type I interferon signaling regulates myeloid and T cell crosstalk in the glioblastoma tumor microenvironment.
查看英文原题
Type I interferon signaling regulates myeloid and T cell crosstalk in the glioblastoma tumor microenvironment.
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中文摘要
通过I型干扰素（IFN）受体IFNAR的下游干扰素信号传导，对于正确产生I型IFN以发起抗肿瘤免疫应答至关重要。我们的研究利用单细胞RNA测序分析TIL（肿瘤浸润淋巴细胞），探讨I型IFN信号传导在胶质母细胞瘤（GBM）肿瘤微环境中的作用。我们研究髓系区室内的I型IFN信号传导如何促进肿瘤微环境中与T细胞的串扰。通过使用Gl261小鼠GBM模型，我们发现缺乏适当的I型IFN应答会导致髓系细胞之间PD-L1相互作用增强，从而影响T细胞功能。此外，我们还通过分析细胞间通讯网络，表征了抗PD1治疗如何诱导肿瘤相关单核细胞和巨噬细胞的转录变化，并提出免疫检查点阻断治疗可能如何缓解部分由缺乏适当I型IFN产生所导致的免疫抑制。
展开英文摘要原文
Downstream interferon signaling through the type I interferon (IFN) receptor, IFNAR, is crucial for the proper production of type I IFNs in mounting anti-tumor immune responses.
Our study investigates the role of type I IFN signaling in the glioblastoma (GBM) tumor microenvironment by leveraging single-cell RNA sequencing to analyze tumor-infiltrating lymphocytes.
We investigate how type I IFN signaling within the myeloid compartment contributes to the crosstalk with T cells in the tumor microenvironment. Through the use of the Gl261 murine GBM model, we find that the lack of proper type I IFN response results in enhanced PD-L1 interactions among myeloid cells, thereby affecting T cell functionality.
Additionally, we also characterize how anti-PD1 treatment induces transcriptional changes in tumor-associated monocytes and macrophages by analyzing intercellular communication networks and propose how immune checkpoint blockade therapy could possibly relieve some of the immunosuppression derived from the lack of proper type I IFN production.
论文信息
- 作者
- Lim J、La J、Kim HC、Kang I、Kang BH、Ku KB、Kim Y、Kwon MS
- 第一作者单位
- Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology (KAIST), Daejeon 34141, Republic of Korea.South Korea
- 通讯作者单位
- Laboratory of Host Defenses, Department of Biological Sciences, KAIST, Daejeon 34141, Republic of Korea.South Korea
- 期刊
- iScience2024 Sep 20
- 原文标识
- PubMed 39286510 · DOI 10.1016/j.isci.2024.110810
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