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现有资料表明,乙型肝炎病毒(HBV)并无细胞病变效应,肝细胞的损伤取决于宿主对受感染肝细胞膜上所表达的病毒抗原和(或)自身抗原的免疫应答,HBV 感染的结局受宿主因素(而不是病毒的数量和毒力)的影响。本文着重讨论 HBV 感染时肝细胞损伤的免疫机理及其研究进展。一、急性肝炎1972年 Dudley 等曾正确地推测,HBV感染后可产生病毒特异性抗原,后者插入肝细胞表面可引起特异性细胞毒性 T 细胞的免疫应答。最近的研究提示,体液免疫能调节T 细胞(TC)对感染 HBV 肝细胞的溶解效应,并控制感染向邻近细胞蔓延。有些实验还提示,多聚人血清白蛋白(pHSA)可以在 HBV 和肝细胞之间充当桥梁,有助于HBV 渗入肝细胞。急性乙型肝炎早期,抗 Dane 颗粒表面决定簇的抗体反应与清除完整的 HBV 颗粒
The available data indicate that hepatitis B virus (HBV) has no cytopathic effect and the damage of hepatocytes depends on the immune response of the host to viral antigens and / or self antigens expressed on the membrane of infected liver cells, and the outcome of HBV infection Affected by host factors (rather than the number and virulence of the virus). This article focuses on the immune mechanism of hepatocellular injury during HBV infection and its research progress. Acute hepatitis Dudley et al. (1972) correctly speculated that HBV-infected mice could produce virus-specific antigens, which inserted into the surface of hepatocytes to cause specific cytotoxic T-cell immune responses. Recent research suggests that humoral immunity regulates the lytic effect of T cells (TCs) on infected HBV hepatocytes and controls the spread of infection to adjacent cells. Some experiments also suggest that poly-serum human serum albumin (pHSA) can act as a bridge between HBV and hepatocytes, helping to infiltrate HBV into hepatocytes. In the early stage of acute hepatitis B, the antibody response to Dane particle surface determinants and the elimination of intact HBV particles