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NAFLD导致选择性CD4 ((+) T淋巴细胞损失,并促进肝癌发生

Chi Ma¹, Aparna H Kesarwala², Tobias Eggert¹

¹Gastrointestinal Malignancy Section, Thoracic and Gastrointestinal Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.

|March 3, 2016

概括

非酒精性脂肪肝 (NAFLD) 通过降低CD4T细胞,加速肝癌的抗瘤免疫力. 通过反应性氧物种 (ROS) 阻断恢复这些细胞可以延缓肝细胞癌 (HCC) 的生长.

科学领域:

免疫学
肝病学
代谢疾病研究

背景情况:

肝细胞癌 (HCC) 是癌症死亡的主要原因.
非酒精性脂肪肝 (NAFLD) 是一个日益严重的公共卫生问题,也是HCC的风险因素.
与NAFLD相关的HCC背后的免疫机制尚不清楚.

研究的目的:

研究适应性免疫在NAFLD促进的HCC中的作用.
确定受NAFLD影响的特定免疫细胞群.
在这种情况下阐明驱动免疫失调的分子机制.

主要方法:

分析小鼠模型和人类肝脏样本.
流细胞测量以评估淋巴细胞数量.
线粒体测定和反应性氧物种 (ROS) 生产的评估.
在体内的实验涉及ROS阻塞.

主要成果:

导致肝脏内CD4 ((+) T细胞的选择性耗尽,而不是CD8 ((+) T细胞.
与CD4 ((+) T细胞相比,它们的线粒体质量和ROS产量更高.
在NAFLD中积累的酸会加剧线粒体功能障碍和CD4 ((+) T细胞损失.
在体内阻断ROS恢复了CD4 ((+) T细胞数量和减弱了HCC的进展.

结论:

在NAFLD中,脂质代谢失调通过选择性CD4 ((+) T细胞损失损害了抗瘤免疫监测.
线粒体功能障碍和ROS在这个过程中起着至关重要的作用.
针对ROS可能为NAFLD相关的HCC提供治疗策略.

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