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首页> 外文期刊>Cancer Cell >Metabolic activation of intrahepatic CD8+ T cells and NKT cells causes nonalcoholic steatohepatitis and liver cancer via cross-talk with hepatocytes
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Metabolic activation of intrahepatic CD8+ T cells and NKT cells causes nonalcoholic steatohepatitis and liver cancer via cross-talk with hepatocytes

机译：肝内CD8 + T细胞和NKT细胞的代谢活化通过与肝细胞的串扰引起非酒精性脂肪性肝炎和肝癌

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摘要

Hepatocellular carcinoma (HCC), the fastest rising cancer in the United States and increasing in Europe, often occurs with nonalcoholic steatohepatitis (NASH). Mechanisms underlying NASH and NASH-induced HCC are largely unknown. We developed a mouse model recapitulating key features of human metabolic syndrome, NASH, and HCC by long-term feeding of a choline-deficient high-fat diet. This induced activated intrahepatic CD8+ Tcells, NKT cells, and inflammatory cytokines, similar to NASH patients. CD8+ Tcells and NKT cells but not myeloid cells promote NASH and HCC through interactions with hepatocytes. NKT cells primarily cause steatosis via secreted LIGHT, while CD8+ and NKT cells cooperatively induce liver damage. Hepatocellular LTβR and canonical NF-κB signaling facilitate NASH-to-HCC transition, demonstrating that distinct molecular mechanisms determine NASH and HCC development.
机译：肝细胞癌（HCC）是美国上升最快的癌症，在欧洲呈上升趋势，通常发生在非酒精性脂肪性肝炎（NASH）中。 NASH和NASH诱导的HCC的潜在机制在很大程度上尚不清楚。我们开发了一种小鼠模型，该模型通过长期喂养胆碱缺乏的高脂饮食来概括人类代谢综合征，NASH和HCC的关键特征。类似于NASH患者，这会诱导活化的肝内CD8 + T细胞，NKT细胞和炎性细胞因子。 CD8 + T细胞和NKT细胞而非髓细胞通过与肝细胞的相互作用促进NASH和HCC。 NKT细胞主要通过分泌的LIGHT引起脂肪变性，而CD8 +和NKT细胞协同诱导肝损伤。肝细胞LTβR和典型的NF-κB信号传导促进NASH向HCC的转变，表明不同的分子机制决定了NASH和HCC的发展。

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