肠道病毒71型调控宿主免疫反应机制的研究进展  

Progress of research in the regulatory mechanism of enterovirus 71 in host immune response

作　　者：池传珍(综述) 孙其玉(综述) 金玉(审校)[1] 

机构地区：[1]南京大学医学院南京医科大学附属南京儿童医院,210008

出　　处：《国际儿科学杂志》2013年第6期613-616,共4页International Journal of Pediatrics

摘　　要：病毒感染可以引起各种宿主免疫反应,防止病毒的扩散传播.固有免疫是宿主抵抗病毒感染的第一道防线,病毒进入机体后,一方面由巨噬细胞吞噬,加工处理病毒抗原,另一方面激活固有的抗病毒免疫应答.肠道病毒71型（EV71）感染诱导干扰素表达可能与细胞特异性应答有关.多数研究表明EV71可以通过多种途径抑制干扰素的表达,以达到免疫逃逸的目的.随后由抗原呈递细胞将抗原信息呈递给T/B细胞,特异性T/B细胞被抗原刺激后活化、增殖、分化为免疫效应细胞,分泌抗体、细胞因子或细胞毒性介质,最终发挥免疫效应.EV71感染过程中体液免疫和细胞免疫均被激活,并在介导保护效应方面起重要作用.细胞免疫应答在防止EV71感染后严重并发症的发展方面起重要作用,而体液免疫产生的中和抗体在EV71感染的保护性免疫方面起关键作用,但是抗体应答水平与疾病严重性并没有相关性.另外,病毒感染时也可以诱导细胞凋亡,阻止病毒增殖和子代病毒的扩散.Virus infection can cause a variety of host immune response to prevent the spreading of virus.Innate immunity is the first line of defense to resist to virus infection in host.After the virus enters,the macrophage phagocytoses and process of virus antigen.On the other hand,it activates the innate antiviral immune response.The expression of interferon after EV71 infection may be associated with cell specific response.Most studies have shown that EV71 can inhibit the expression of interferon to achieve immune escape.Then antigen presenting cells present antigens to T/B lymphocytes,once specific T/B lymphocytes are activated by antigen,they will be activated,proliferated,diferentiated to immunologic effector cells,which secrete antibodies,cytokines,cell toxicity of medium,ultimately,develop immunological effect.Both humoral immunity and cellular immunity are activated in EV71 infection,and play an important role in mediating protection effect.Cellular immunity may be associated with the clinical outcome of EV71 infection.The EV71-specific neutralizing antibody generated by the humoral immunity plays a key role in protective immunity,but the antibody response level is not correlated with disease severity.In addition,virus infection can induce cell apoptosis to prevent the virus proliferation and the spreading of progeny virus.

关 键 词：肠道病毒71型 宿主免疫 细胞因子 凋亡 

分 类 号：R512.5[医药卫生—内科学]