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首页> 外文期刊>Hepatology: Official Journal of the American Association for the Study of Liver Diseases >Biliary epithelial cells and primary biliary cirrhosis: The role of liver-infiltrating mononuclear cells
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Biliary epithelial cells and primary biliary cirrhosis: The role of liver-infiltrating mononuclear cells

机译：胆道上皮细胞和原发性胆汁性肝硬化：肝浸润单个核细胞的作用

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摘要

Primary biliary cirrhosis (PBC) is characterized by the highly selective autoimmune injury of small intrahepatic bile ducts, despite widespread distribution of mitochondrial autoantigens. On this basis, it has been suggested that the targeted biliary epithelial cells (BECs) play an active role in the perpetuation of autoimmunity by attracting immune cells via chemokine secretion. To address this issue, we challenged BECs from patients with PBC and controls using multiple Toll-like receptor (TLR) ligands as well as autologous liver-infiltrating mononuclear cells (LMNCs) with subsequent measurement of BEC phenotype and chemokine production and LMNC chemotaxis by quantifying specific chemokines. Our data reflect that BECs from PBC patients and controls express similar levels of TLR subtypes, CD40, and human leukocyte antigen DR alpha (HLA-DR alpha) and produce equivalent amounts of chemokines in our experimental conditions. Interestingly, however, BEC-expressed chemokines elicit enhanced transmigration of PBC LMNCs compared with controls. Furthermore, the addition of autologous LMNCs to PBC BECs led to the production of higher levels of chemokines and enhanced the expression of CD40 and HLA-DR alpha. Conclusion: We submit that the proinflammatory activity of BECs in PBC is secondary to the intervention of LMNCs and is not determined per se. These data support the hypothesis that BECs are in fact "innocent victims" of autoimmune injury and that the adaptive immune response is critical in PBC.
机译：尽管线粒体自身抗原广泛分布，原发性胆汁性肝硬化（PBC）的特征是肝内小胆管的高度选择性自身免疫损伤。在此基础上，已经提出，靶向胆管上皮细胞（BEC）通过趋化因子分泌吸引免疫细胞，在自身免疫永存中发挥积极作用。为了解决这个问题，我们使用多个Toll样受体（TLR）配体以及自体肝浸润性单核细胞（LMNC）挑战了PBC和对照患者的BEC，随后通过定量测量BEC表型和趋化因子的产生以及LMNC趋化性特定趋化因子。我们的数据反映，来自PBC患者和对照的BEC在我们的实验条件下表达相似水平的TLR亚型，CD40和人白细胞抗原DRα（HLA-DR alpha），并产生等量的趋化因子。然而，有趣的是，与对照相比，BEC表达的趋化因子引起PBC LMNCs的转运增强。此外，在PBC BEC中添加自体LMNC导致产生更高水平的趋化因子，并增强CD40和HLA-DRα的表达。结论：我们认为，PEC中BEC的促炎活性仅次于LMNCs的干预，尚不能确定。这些数据支持以下假设：BEC实际上是自身免疫损伤的“无辜受害者”，而适应性免疫应答在PBC中至关重要。

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