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改变的NCR3拼接变异可能导致细胞癌患者的NK细胞功能缺陷

Xuelei Wang¹, Liqun Huang¹, Xiaofei Wen¹

¹Department of Urology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, P.R. China.

In vivo (Athens, Greece)

|December 26, 2023

概括

在细胞癌 (RCC) 患者中,自然杀手细胞 (NK) 缺乏与免疫刺激性NCR3拼接变体的表达减少有关. 这有助于免疫逃逸和不良预后,建议新的治疗点.

科学领域:

免疫学免疫学免疫学
在瘤学瘤学.
分子生物学分子生物学

背景情况:

自然杀手 (NK) 细胞功能障碍可能会抑制恶性瘤患者的抗瘤免疫力.
细胞癌 (RCC) 的预后通常很差,原因是瘤细胞从NK细胞细胞毒性中逃脱,特别是涉及自然细胞毒性受体 (NCR).

研究的目的:

调查NCRs,特别是NCR3拼接变体在RCC患者观察到的NK细胞缺陷中的作用.
在细胞癌的背景下探索NK细胞功能障碍的潜在机制.

主要方法:

流细胞计用于分析RCC患者的外周血液和瘤组织中的NK细胞表型.
抗体依赖细胞中介细胞毒性 (ADCC) 测定测量NKp30中介NK细胞杀死功能.
实时定量PCR检测到NKp30拼接变体 (NKp30a,NKp30b,NKp30c) 和细胞因子 (IL-6,IL-8,IL-10,IL-18,TGF-β) 的mRNA水平.

主要成果:

RCC患者在瘤组织中NK细胞的比例降低,最显著的是影响NKp30+NK细胞.
在RCC患者中,NKp30+NK细胞介导的细胞毒性是有限的,正如ADCC测定所示.
在RCC患者中观察到免疫刺激性NCR3拼接变体 (NKp30a,NKp30b) 的表达较低,以及激活性细胞因子 (IL-6,IL-8) 和不变的抑制性细胞因子 (TGF-β) 表达的减少,从而创造了一个免疫抑制的微环境.

结论:

免疫刺激性NCR3拼接变体的减少表达和抑制性细胞因子微环境有助于RCC中缺乏NK细胞细胞毒性.
这些因素有助于癌细胞从NK细胞介导的杀死中获得免疫逃脱.
这些发现为开发RCC新型免疫治疗点提供了理论基础.

关键词:

在 NCR3 中, NCR3 是一个 NCR3 类型.在 NK 细胞中, NK 细胞是最重要的.细胞癌是细胞癌.细胞因子微环境拼接的变种拼接的变种

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RNA Splicing

RNA Splicing

Splicing is the process by which eukaryotic RNA is edited before its translation into protein. The RNA strand transcribed from eukaryotic DNA is called the primary transcript. The primary transcripts that become mRNAs are called precursor messenger RNAs (pre-mRNAs). Eukaryotic pre-mRNA contains alternating sequences of exons and introns. Exons are nucleotide sequences that code for proteins, whereas introns are the non-coding regions. In RNA splicing, introns are removed and exons are bonded...