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NAFLD causes selective CD4(+) T lymphocyte loss and promotes hepatocarcinogenesis

機(jī)譯：NAFLD導(dǎo)致選擇性CD4（+）T淋巴細(xì)胞丟失并促進(jìn)肝癌發(fā)生

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摘要

Hepatocellular carcinoma (HCC) is the second most common cause of cancer-related death. Non-alcoholic fatty liver disease (NAFLD) affects a large proportion of the US population and is considered to be a metabolic predisposition to liver cancer. However, the role of adaptive immune responses in NAFLD-promoted HCC is largely unknown. Here we show, in mouse models and human samples, that dysregulation of lipid metabolism in NAFLD causes a selective loss of intrahepatic CD4(+) but not CD8(+) T lymphocytes, leading to accelerated hepatocarcinogenesis. We also demonstrate that CD4(+) T lymphocytes have greater mitochondrial mass than CD8(+) T lymphocytes and generate higher levels of mitochondrially derived reactive oxygen species (ROS). Disruption of mitochondrial function by linoleic acid, a fatty acid accumulated in NAFLD, causes more oxidative damage than other free fatty acids such as palmitic acid, and mediates selective loss of intrahepatic CD4(+) T lymphocytes. In vivo blockade of ROS reversed NAFLD-induced hepatic CD4(+) T lymphocyte decrease and delayed NAFLD-promoted HCC. Our results provide an unexpected link between lipid dysregulation and impaired anti-tumour surveillance.

機(jī)譯：肝細(xì)胞癌（HCC）是與癌癥相關(guān)的死亡的第二大最常見(jiàn)原因。非酒精性脂肪肝疾?。∟AFLD）影響著美國(guó)大部分人口，被認(rèn)為是肝癌的代謝易感性。然而，在NAFLD促進(jìn)的肝癌中適應(yīng)性免疫反應(yīng)的作用在很大程度上尚不清楚。在這里，我們顯示，在小鼠模型和人類(lèi)樣品中，NAFLD中脂質(zhì)代謝的失調(diào)導(dǎo)致肝內(nèi)CD4（+）而不是CD8（+）T淋巴細(xì)胞的選擇性丟失，從而導(dǎo)致肝癌的加速發(fā)生。我們還證明了CD4（+）T淋巴細(xì)胞比CD8（+）T淋巴細(xì)胞具有更大的線(xiàn)粒體質(zhì)量，并產(chǎn)生更高水平的線(xiàn)粒體來(lái)源的活性氧（ROS）。亞油酸（一種堆積在NAFLD中的脂肪酸）破壞線(xiàn)粒體功能，比其他游離脂肪酸（如棕櫚酸）引起更多的氧化損傷，并介導(dǎo)肝內(nèi)CD4（+）T淋巴細(xì)胞的選擇性損失。 ROS的體內(nèi)阻滯逆轉(zhuǎn)了NAFLD誘導(dǎo)的肝CD4（+）T淋巴細(xì)胞減少并延遲了NAFLD促進(jìn)的HCC。我們的結(jié)果為脂質(zhì)失調(diào)與抗腫瘤監(jiān)測(cè)受損之間提供了意料之外的聯(lián)系。