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首页> 外文期刊>Immunity >Interleukin-13 Activates Distinct Cellular Pathways Leading to Ductular Reaction, Steatosis, and Fibrosis
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Interleukin-13 Activates Distinct Cellular Pathways Leading to Ductular Reaction, Steatosis, and Fibrosis

机译：白介素13激活不同的细胞途径，导致导管反应，脂肪变性和纤维化

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Fibroproliferative diseases are driven by dysregulated tissue repair responses and are a major cause of morbidity and mortality because they affect nearly every organ system. Type 2 cytokine responses are critically involved in tissue repair; however, the mechanisms that regulate beneficial regeneration versus pathological fibrosis are not well understood. Here, we have shown that the type 2 effector cytokine interleukin-13 simultaneously, yet independently, directed hepatic fibrosis and the compensatory proliferation of hepatocytes and biliary cells in progressive models of liver disease induced by interleukin-13 overexpression or after infection with Schistosoma mansoni. Using transgenic mice with interleukin-13 signaling genetically disrupted in hepatocytes, cholangiocytes, or resident tissue fibroblasts, we have revealed direct and distinct roles for interleukin-13 in fibrosis, steatosis, cholestasis, and ductular reaction. Together, these studies show that these mechanisms are simultaneously controlled but distinctly regulated by interleukin-13 signaling. Thus, it may be possible to promote interleukin-13-dependent hepatobiliary expansion without generating pathological fibrosis.
机译：纤维增生性疾病是由组织修复反应失调驱动的，是发病率和死亡率的主要原因，因为它们几乎影响每个器官系统。 2型细胞因子反应与组织修复至关重要。然而，调节有益再生与病理性纤维化的机制尚不十分清楚。在这里，我们已经显示，在由白细胞介素13过度表达或曼氏血吸虫感染诱发的肝病进行性模型中，2型效应细胞因子白细胞介素13同时但独立地指导肝纤维化以及肝细胞和胆道细胞的代偿性增生。使用具有在肝细胞，胆管细胞或常驻组织成纤维细胞中基因突变的白介素13信号转基因的小鼠，我们已经揭示了白介素13在纤维化，脂肪变性，胆汁淤积和导管反应中的直接作用。总之，这些研究表明，这些机制同时受白介素13信号控制，但受到明显调节。因此，有可能促进白介素13依赖性肝胆扩张而不产生病理性纤维化。

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