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炎症小体和细胞因子在肝硬化免疫功能障碍中的作用。

Role of inflammasomes and cytokines in immune dysfunction of liver cirrhosis.

机构信息

Dept. of Bioengineering & Technology, Gauhati University, Assam 781014, India.

Dept. of Bioengineering & Technology, Gauhati University, Assam 781014, India.

出版信息

Cytokine. 2023 Oct;170:156347. doi: 10.1016/j.cyto.2023.156347. Epub 2023 Aug 26.

Abstract

Liver cirrhosis develops as a result of persistent inflammation and liver injury. The prolonged inflammation triggers the buildup of fibrous tissue and regenerative nodules within the liver, leading to the distortion of the hepatic vascular structure and impaired liver function. Cirrhosis disrupts the ability of liver function to maintain homeostasis and hepatic immunosurveillance which causes immunological dysfunction in the body. In pathological conditions, the production of cytokines in the liver is carefully regulated by various cells in response to tissue stimulation. Cytokines and inflammasomes are the key regulators and systematically contribute to the development of cirrhosis which involves an inflammatory response. However, the crosstalk role of different cytokines in the cirrhosis progression is poorly understood. Tumour necrosis factor-alpha (TNF-α), interleukin-1 (IL-1), interleukin-6 (IL-6), and interferon-gamma (IFN-γ), among others, are proinflammatory cytokines that contribute to liver cell necrosis, which in turn causes the development of fibrosis. While IL-10 exhibits a potent anti-inflammatory effect on the liver by inhibiting immune cell activation and neutralizing pro-inflammatory cytokine activity. Inflammasomes have also been implicated in the profibrotic processes of liver cirrhosis, as well as the production of chemokines such as CCL2/MCP-1. It is evident that inflammasomes have a role in the proinflammatory response seen in chronic liver illnesses. In conclusion, cirrhosis significantly impacts the immune system, leading to immunological dysfunction and alterations in both innate and acquired immunity. Proinflammatory cytokines like TNF-α, IL-1β, IL-6, and IFNγ are upregulated in cirrhosis, contributing to liver cell necrosis and fibrosis development. Managing cytokine-mediated inflammation and fibrosis is a key therapeutic approach to alleviate portal hypertension and its associated liver complications. This review attempted to focus largely on the role of immune dysfunction mediated by different cytokines and inflammasomes involved in the progression, regulation and development of liver cirrhosis.

摘要

肝硬化是由于持续性炎症和肝损伤引起的。长期的炎症会触发肝脏内纤维组织和再生结节的堆积,导致肝血管结构扭曲和肝功能受损。肝硬化破坏了肝脏维持内环境稳定和肝免疫监视的能力,导致机体免疫功能障碍。在病理条件下,肝脏中细胞因子的产生受到各种细胞的精细调节,以响应组织刺激。细胞因子和炎性小体是关键的调节因子,系统性地参与了肝硬化的发生发展,涉及炎症反应。然而,不同细胞因子在肝硬化进展中的相互作用作用机制尚不清楚。肿瘤坏死因子-α(TNF-α)、白细胞介素-1(IL-1)、白细胞介素-6(IL-6)和干扰素-γ(IFN-γ)等促炎细胞因子有助于肝细胞坏死,进而导致纤维化的发展。而白细胞介素-10(IL-10)通过抑制免疫细胞激活和中和促炎细胞因子活性,对肝脏具有强大的抗炎作用。炎性小体也参与了肝硬化的纤维化过程,以及趋化因子如 CCL2/MCP-1 的产生。炎性小体在慢性肝病中的促炎反应中起作用是显而易见的。总之,肝硬化对免疫系统有重大影响,导致免疫功能障碍和固有免疫和获得性免疫的改变。TNF-α、IL-1β、IL-6 和 IFNγ等促炎细胞因子在肝硬化中上调,导致肝细胞坏死和纤维化发展。管理细胞因子介导的炎症和纤维化是缓解门脉高压及其相关肝脏并发症的关键治疗方法。本综述主要试图关注不同细胞因子和炎性小体在肝硬化的进展、调节和发展过程中所介导的免疫功能障碍的作用。

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