自介导的NKG2D内部化会损害NK细胞的功能,并加剧辐射性肺炎
Ruiqing Wang1, Xinyue Ma1, Xinyu Zhang1
1Qilu Hospital of Shandong University, Cheeloo College of Medicine, Shandong University, Jinan, China.
Frontiers in immunology
|December 11, 2023
概括
辐射性肺炎通过过度的自会损害自然杀手 (NK) 细胞的功能,导致肺损伤. 调节自和增强NK细胞活性可以治疗这种情况.
科学领域:
- 免疫学 免疫学 免疫学
- 在瘤学瘤学.
- 肺部病理学 肺部病理学
背景情况:
- 放射性肺炎是胸部放射治疗的严重并发症,导致严重的呼吸道疾病.
- 自然杀手 (NK) 细胞在辐射肺炎病原体中的确切作用尚不清楚.
研究的目的:
- 调查NK细胞在辐射肺炎中的参与和功能状态.
- 阐明这种情况NK细胞功能障碍的潜在机制.
主要方法:
- 在放射性肺炎患者和动物模型中分析NK细胞的存在和功能.
- 利用免疫光学,西部涂抹和免疫沉来评估CXCL10,ROS,自和NKG2D受体动力学.
主要成果:
- 在辐射肺炎组织中观察到NK细胞透率增加但功能减弱.
- 在动物模型中增强NK细胞活性减缓了疾病的进展.
- 增加的CXCL10和ROS水平与疾病进展相关;患者NK细胞过度自与ROS积累有关.
- 辐射暴露加剧了NKG2D受体,适应蛋白和溶酶体之间的相互作用,导致NKG2D降解.
结论:
- 辐射诱导的肺损伤通过一种依赖于自的途径抑制NK细胞功能.
- 向自和增强NK细胞活性是辐射肺炎的潜在治疗策略.
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