B型肝炎病毒e蛋白的免疫調節作用

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Title:	B型肝炎病毒e蛋白的免疫調節作用
Other Titles:	Immunomodulatory Function of the e Protein of Hepatitis B Virus
Authors:	胡承波 Hu, Cheng-po
Contributors:	行政院國家科學委員會東海大學生物系
Date:	2006
Issue Date:	2011-06-15T08:33:41Z (UTC)
Abstract:	B型肝炎病毒的感染會導致急性或慢性肝炎，而慢性B型肝炎病毒的帶原者有很高的機率會演變成肝硬化或是肝癌。在病毒與宿主共演化的過程中，病毒逐漸發展出特殊的方式來干擾宿主的免疫系統，以達到慢性感染的目的。B型肝炎病毒的e蛋白不存在於病毒顆粒中，和病毒的複製也沒有直接的關聯，所以被認為可能和干擾宿主的免疫反應有關。Kupffer細胞是肝臟內的巨噬細胞，不但具有呈現抗原(antigen presentation)的功能，也被認為與肝臟內免疫反應的調控有關。本研究顯示e蛋白可以和小鼠的Kupffer細胞結合，並且也發現e蛋白可以誘使小鼠Kupffer細胞產生多種細胞激素，如IL-1、IL-6、 IL-10、TNF-α、TGF-β、MIP-2及MCP-1。其次我們也發現e蛋白會影響T細胞的功能及抗體的產生。在利用植物血凝素 (phytohemagglutinin, PHA) 刺激T細胞增生的實驗中，我們發現e蛋白會使Kupffer細胞呈現抗原的能力降低。在小鼠對抗B型肝炎病毒表面抗原的實驗中顯示e蛋白並不會影響對抗HBsAg的總IgG量，但卻明顯地抑制了對抗HBsAg的IgG2a 。綜合以上結果，e蛋白可以誘發Kupffer細胞產生細胞激素及影響宿主的T細胞及抗體反應，藉由此功能可能可以助長病毒的潛伏及慢性感染。 Hepatitis B virus (HBV) is a hepatotropic, noncytopathic virus that causes acute and chronic necroinflammatory liver diseases. Chronic HBV carriers serve as a source for new infections and are at a high risk of developing liver cirrhosis and hepatocellular carcinoma (HCC). To establish a chronic infection, viruses have developed strategies to evade host immune system. HBe protein is not a structural component of the HBV, nor is required for the viral infectivity and replication. It may play an immunomodulatory role in the life cycle of HBV. Kupffer cells are the resident macrophages in the liver and can function as antigen-presenting cells. It has been suggested that Kupffer cells are involved in the regulation of intrahepatic immune responses. To study if HBe protein may modulate the function of Kupffer cells and further affect host anti-HBV immunity, we examined the interaction between HBe protein and Kupffer cells and further investigated the effect of HBe protein on T cell proliferation and antibody production. We showed that HBe protein could bind to Kupffer cells, and HBe protein was able to trigger the expression of IL-1, IL-6, IL-10, TNF-α, TGF-β, MIP-2, and MCP-1 in Kupffer cells. We also demonstrated that HBe decreased the antigen presenting ability of Kupffer cells in a PHA-stimulated T cell proliferation assay. Furthermore, the amount of anti-HBs IgG2a was significantly decreased in HBe-treated mice although the total anti-HBs IgG was the same in HBe-treated and control mice. Taken together, our results suggest that HBe may modulate the function of Kupffer cells and modify the anti-HBV immune responses. These effects may result in ineffective viral clearance and establishment of persistent infection.
Relation:	研究編號NSC95-2320-B029-001-MY3 研究期間：2006-08 ~ 2007-07
Appears in Collections:	[Department of Life Sciences ] National Research Council Report

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