摘要
细胞因子和趋化因子,丙型肝炎病毒(HCV)感染诱导,参与病毒控制和肝损伤。在感染初期操作的细胞因子网络能够协调和有效地发展先天和适应性免疫应答。HCV通过诱导T辅助细胞(Th)2或者T细胞毒性2细胞因子谱来干扰各种细胞因子并躲避免疫应答。Th1免疫反应(与细胞因子相关)优势已经在慢性肝炎C感染和肝外表现中得到证实。干扰素(IFN)-γ和IFN-γ诱导型趋化因子(C-X-C基因)配体(CXCL)9,10和11由于不能控制感染过程而引起炎症浸润肝实质,并导致了广泛的肝损伤和肝硬化。最重要的系统性HCV相关的肝外疾病——混合型低血球蛋白血症、淋巴增生紊乱,糖尿病以及自身免疫性甲状腺疾病紊乱与细胞因子/趋化因子网络的复杂失调相关,并涉及促炎症和Th1趋化因子。细胞因子如IFN-α的治疗性给可能会导致在持续感染期间的病毒清除以及恢复“降低循环CXCL10水平”的过程。几项研究报道了白介素(IL)-28B多态性,循环CXCL-10在HCV感染中可能是HCV治疗有效性的预后指标。也有其他研究报道展示了通过直接抗病毒试剂治疗来清除HCV增加了循环CXCL10的水平。理论上选择性试剂中和CXCL10能够增加患者对传统的基于IFN的HCV治疗的反应性,同时减少炎性免疫细胞活化。
关键词: 趋化因子,CXCL10,细胞因子,IFN诱导的细胞因子,HCV肝外表现,肝炎C慢性感染,肝炎C病毒
Current Drug Targets
Title:Chemokines in the Pathogenesis and as Therapeutical Markers and Targets of HCV Chronic Infection and HCV Extrahepatic Manifestations
Volume: 18 Issue: 7
关键词: 趋化因子,CXCL10,细胞因子,IFN诱导的细胞因子,HCV肝外表现,肝炎C慢性感染,肝炎C病毒
摘要: Cytokines and chemokines, hepatitis C virus (HCV) infection-induced, participate in viral control and liver damage. The complex cytokine network, operating during initial infection allows a coordinated and effective development of innate and adaptive immune responses. “HCV interferes with cytokines at various levels and escapes immune response by inducing a T helper (Th)2/T cytotoxic 2 cytokine profile”. A predominance of the Th1 immune response (and related cytokines) has been evidenced in chronic hepatitis C infection and in extrahepatic manifestations. Interferon (IFN)-γ and IFN-γ-inducible chemokine (C-X-C motif) ligand (CXCL)9, -10 and -11 recruit inflammatory infiltrates into the liver parenchyma due to the incapability to control the infection process, resulting in extensive liver damage and liver cirrhosis. “The most important systemic HCV-related extrahepatic diseases — mixed cryoglobulinemia, lymphoproliferative disorders, diabetes and autoimmune thyroid disorders — are associated with a complex dysregulation of the cytokine/chemokine network and involve pro-inflammatory and Th1 chemokines. The therapeutical administration of cytokines such as IFN-α may result in viral clearance during persistent infection and reverts this process” reducing circulating CXCL10 levels. “Several studies have reported interleukin (IL)-28B polymorphisms, and circulating CXCL10, may be prognostic markers for HCV treatment efficacy in HCV infection”. Other studies have also shown that HCV clearance by directly acting antiviral agents therapy decreases circulating CXCL10 levels. “Theoretically agents that selectively neutralize CXCL10 could increase patient responsiveness to traditional IFN-based HCV therapy”, simultaneously reducing inflammatory immune cell activation.
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Chemokines in the Pathogenesis and as Therapeutical Markers and Targets of HCV Chronic Infection and HCV Extrahepatic Manifestations, Current Drug Targets 2017; 18 (7) . https://dx.doi.org/10.2174/1389450116666150804105937
DOI https://dx.doi.org/10.2174/1389450116666150804105937 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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