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首页> 美国卫生研究院文献>International Journal of Molecular Sciences >Dendritic Cell and T Cell Crosstalk in Liver Fibrogenesis and Hepatocarcinogenesis: Implications for Prevention and Therapy of Liver Cancer
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Dendritic Cell and T Cell Crosstalk in Liver Fibrogenesis and Hepatocarcinogenesis: Implications for Prevention and Therapy of Liver Cancer

机译：肝纤维发生和肝癌发生中的树突状细胞和T细胞串扰：对肝癌预防和治疗的影响

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摘要

Liver fibrosis is a chronic, highly prevalent disease that may progress to cirrhosis and substantially increases the risk for development of hepatocellular carcinoma (HCC). Fibrotic livers are characterized by an inflammatory microenvironment that is composed of various immunologically active cells, including liver-resident populations (e.g., Kupffer cells, hepatic stellate cells and sinusoidal endothelium) and infiltrating leukocytes (e.g., monocytes, monocyte-derived macrophages, neutrophils and lymphocytes). While inflammatory injury drives both fibrogenesis and carcinogenesis, the tolerogenic microenvironment of the liver conveys immunosuppressive effects that encourage tumor growth. An insufficient crosstalk between dendritic cells (DCs), the professional antigen presenting cells, and T cells, the efficient anti-tumor effector cells, is one of the main mechanisms of HCC tumor tolerance. The meticulous analysis of patient samples and mouse models of fibrosis-HCC provided in-depth insights into molecular mechanisms of immune interactions in liver cancer. The therapeutic modulation of this multifaceted immunological response, e.g., by inhibiting immune checkpoint molecules, in situ vaccination, oncolytic viruses or combinations thereof, is a rapidly evolving field that holds the potential to improve the outcome of patients with HCC. This review aims to highlight the current understanding of DC–T cell interactions in fibrogenesis and hepatocarcinogenesis and to illustrate the potentials and pitfalls of therapeutic clinical translation.
机译：肝纤维化是一种慢性，高度普遍的疾病，可能对肝硬化进行，并且大大提高了肝细胞癌（HCC）的发育风险。纤维化肝脏的特征在于由各种免疫活性细胞组成的炎症微环境，包括肝脏居民（例如，Kupffer细胞，肝星状细胞和正弦内皮）和渗透白细胞（例如单核细胞，单核细胞衍生的巨噬细胞，中性粒细胞和淋巴细胞）。虽然炎症损伤驱动纤维发生和致癌，但肝脏的耐受性微环境传达促进肿瘤生长的免疫抑制作用。树突细胞（DCS），专业抗原呈递细胞和T细胞，有效的抗肿瘤效应细胞的不足串扰是HCC肿瘤耐受性的主要机制之一。纤维化-HCC患者样品和小鼠模型的细致分析提供了深入了解肝癌免疫相互作用的分子机制。这种多方面免疫应答的治疗调节例如通过抑制免疫检查点分子原位疫苗接种，溶于溶解病毒或其组合，是一种快速发展的领域，其具有改善HCC患者患者的潜力。本综述旨在突出目前对纤维发生和肝癌发生中的DC-T细胞相互作用的理解，并说明治疗临床翻译的潜在和缺陷。

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