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IL-10和IL-17在慢性乙型肝炎、乙型肝炎肝硬化以及肝硬化合并腹腔感染中的研究进展 被引量:23

Progress in research of IL-10 and IL-17 in chronic hepatitis B, hepatitis B virus-related liver cirrhosis and cirrhosis with abdominal infection
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摘要 乙型肝炎是全球性的传染性疾病,严重威胁着人类健康.但其致病机制及最终形成肝硬化的机制尚不完全清楚.阐明乙型肝炎病情进展及肝硬化形成的机制成为抗病毒及抗纤维化治疗的重要依据之一.近年来慢性乙型肝炎及肝硬化的发生机制及治疗取得了很大进展,细胞因子成为研究的热点.新出现的证据表明肝内多种细胞因子在乙型肝炎的进行性发展过程中有很重要的作用,细胞因子多通过旁分泌形式介导细胞-细胞相互作用或通过反馈作用自身等形式参与慢性乙型肝炎、肝硬化以及肝硬化合并感染的过程.近年来诸多研究认为血清白介素-10(interleukin 10,IL-10)和IL-17水平的高低与慢性乙型肝炎、乙型肝炎肝硬化及肝硬化合并感染的发生发展及预后有关,本文就IL-10和IL-17对于慢性乙型肝炎、乙型肝炎肝硬化及肝硬化合并感染目前的研究情况进行综述. Hepatitis B is a global contagious disease, pos- ing a serious threat to human health. How- ever, its pathogenic mechanisms and how it ultimately leads to the formation of cirrhosis are not fully understood. Elucidating the pro- gression of hepatitis B and the mechanism re- sponsible for liver cirrhosis formation can help develop novel antiviral treatment and anti- fibrosis therapy. In recent years, great progress has been made in understanding the pathogen- esis of chronic hepatitis and liver cirrhosis and their treatment. Cytokines have become a re- search hotspot in this field. Emerging evidence suggests that a variety of cytokines in the liver have a quite significant role in the progressive process of HBV. Cytokines mainly mediate cell- cell interactions in paracrine, feedback or other manners to participate in the pathogenesis of chronic hepatitis B, cirrhosis and cirrhosis with infection. In recent years, many studies sug- gest that serum interleukin-10 (IL-10) and IL-17 levels are correlated with the development and prognosis of chronic hepatitis B, liver cirrhosis and cirrhosis with infection. In this paper, we review the progress in research of IL-10 and IL-17 in chronic hepatitis B, liver cirrhosis and cirrhosis with infection.
作者 何文敏 苏毅
出处 《世界华人消化杂志》 CAS 北大核心 2014年第3期333-339,共7页 World Chinese Journal of Digestology
基金 贵州省遵义市科技计划基金资助项目 No.遵市科合社字(2011)32~~
关键词 慢性乙型肝炎 肝硬化 感染 细胞因子 白介素-10 白介素-17 Hepatitis B Live cirrhosis Infection Cytokines interleukin i0 Interleukin 17
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