人巨细胞病毒感染中的细胞免疫机制

人巨细胞病毒(HCMV)在人群中普遍易感,免疫力正常者多为隐性感染,可终身携带病毒.感染后,病毒激活机体免疫系统,产生病毒清除作用.在机体清除HCMV的免疫应答中,与机体其他免疫相比,固有免疫中的免疫细胞和获得性免疫中的细胞免疫起着更为重要的作用,同时巨细胞病毒也通过一系列的逃逸反应来对抗上述免疫的清除作用.     

疫苗——抵御疾病的健康卫士

<正>疫苗是指用于人或其他动物，使其免于某种特定病原体，如细菌、病毒和其他微生物等侵害并引发疾病的物质。疫苗可促使机体产生免疫应答，让机体产生能对抗特定病原体的抗体蛋白，进而阻止机体发生感染。     

慢性乙型肝炎免疫治疗的研究

乙型肝炎病毒(HBV)、病毒感染的肝细胞及机体免疫应答三者的相互作用取决于慢性乙肝患者疾病的进展和预后.其中机体的免疫应答是影响疾病进展和抗乙肝病毒治疗疗效的关键.通过对慢性乙型肝炎患者免疫调节治疗,可以恢复及提高机体抗病毒免疫应答能力,从而达到控制及清除病毒的目的.     

硒对人体健康影响研究进展

硒是人体必需微量元素,在体内以硒代半胱氨酸形式编码合成硒蛋白发挥作用。硒及硒蛋白具有抗氧化、免疫调节等广泛生理功能,缺硒与心脑血管疾病、癌症、糖尿病、神经系统疾病、自身免疫性疾病以及传染病等40多种人类疾病有关。硒营养状况与病毒性疾病密切相关,缺硒导致机体氧化还原及免疫调节失衡,促进病毒感染和复制。缺硒引起氧化应激增加病毒基因组突变率。感染病毒的宿主启动抗氧化和免疫应答反应消耗大量硒,病毒本身表达硒蛋白竞争宿主硒源的同时负反馈调节抑制病毒复制。硒作为治疗药物时,应综合考虑患者硒安全剂量水平以及不同硒化合物的毒性差异。最新研究提示硒状态与新型冠状病毒的感染和病程有关,未来需要结合更多的临床和基础研究数据,探索硒对新冠肺炎（COVID-19）在内的病毒感染疾病的影响。     

辅助性T细胞17及调节性T细胞的平衡与人类免疫缺陷病毒感染

辅助性T细胞17(Th17)和调节性T细胞(Treg细胞)均来源于CD4+T细胞,在机体免疫应答中的作用基本相反,Th17促进免疫应答,而Treg细胞抑制免疫应答,正常情况下两者之间的平衡状态有利于保持机体免疫平衡.HIV感染可能打破两者之间的平衡从而导致疾病进展,而HAART可能恢复二者平衡关系.此文就Th17和Treg细胞的平衡状态与HIV感染的关系作了综述.     

Toll样受体3抗乙型肝炎病毒慢性持续感染的进展

目前,HBV慢性持续感染的致病机制仍不明确,多倾向于机体对病毒产生免疫耐受,固有免疫及适应性免疫应答不佳所致.免疫调节治疗有望成为治疗HBV慢性持续性感染的重要手段.Toll样受体3(TLR3)作为病毒双链RNA(dsRNA)识别受体在机体抗病毒免疫中发挥十分重要的作用.此文将对TLR3在HBV慢性持续感染中的作用研究进展作一综述.     

乙型肝炎疫苗佐剂与Th1/Th2细胞平衡调节

日渐增多的证据表明,接种乙型肝炎疫苗后机体保护性免疫应答的产生及感染HBV后机体能否有效清除病毒与Th1/Th2细胞平衡密切相关。一般认为,Th1免疫应答与胞内感染的免疫性和防御性有关,而Th2应答则与感染慢性化有关。因此,在应用乙型肝炎疫苗免疫机体时,若能辅以某种佐剂,调节Th1/Th2细胞平衡,使之诱导机体产生以Th1型应答为主的免疫反应,将有助于有效预防及治疗HBV感染。     

硒抗病毒作用研究进展

硒是人体必需微量元素,在体内以硒代半胱氨酸形式编码合成硒蛋白发挥作用。硒及硒蛋白具有抗氧化、免疫调节等广泛生理功能,缺硒与心脑血管疾病、癌症、糖尿病、神经系统疾病、自身免疫性疾病以及传染病等40多种人类疾病有关。硒营养状况与病毒性疾病密切相关,缺硒导致机体氧化还原及免疫调节失衡,促进病毒感染和复制。缺硒引起氧化应激增加病毒基因组突变率。感染病毒的宿主启动抗氧化和免疫应答反应消耗大量硒,病毒本身表达硒蛋白竞争宿主硒源的同时负反馈调节抑制病毒复制。硒作为治疗药物时,应综合考虑患者硒安全剂量水平以及不同硒化合物的毒性差异。最新研究提示硒状态与新型冠状病毒的感染和病程有关,未来需要结合更多的临床和基础研究数据,探索硒对新冠肺炎(COVID-19)在内的病毒感染疾病的影响。     

免疫系统在乙型、丙型病毒性肝炎发病过程中作用研究进展

乙型病毒性肝炎和丙型病毒性肝炎分别由乙型肝炎病毒和丙型肝炎病毒感染所致。乙型肝炎病毒（HBV）、丙型肝炎病毒（HCV）感染呈全球分布,我国是高流行地区,由于HBV、HCV基因的高变性,容易逃避机体免疫系统的清除。HBV、HCV感染免疫系统细胞,造成机体对HBV、HCV感染的免疫应答异常,并引起组织的损伤,导致肝细胞的慢性持续性感染,并可进一步发展成肝硬化,甚至肝细胞肝癌。HBV、HCV主要经血液传播,包括输血与血制品传播、静脉吸毒、针刺、医源性传播、性接触和母婴垂直传播。     

Th17和Treg细胞的平衡状态与肺结核的关系

Th17和Treg细胞均来源于CD4+T细胞,在机体免疫应答中的作用基本相反,Th17促进免疫应答,而Treg细胞抑制免疫应答,正常情况下两者之间的平衡状态有利于保持机体免疫平衡.结核分枝杆菌感染可能打破两者之间的平衡从而导致疾病进展,而抗结核治疗可能恢复二者平衡关系.此文就Th17和Treg细胞的分化、调控和功能,以及两者在艾滋病及肺结核患者中的变化等进行综述.     

手足口病患儿肠道病毒71感染相关免疫功能变化及其临床意义

手足口病(HFMD)患儿肠道病毒71 (EV71)感染可导致中枢神经、呼吸系统损害,引发脑炎、急性弛缓性麻痹、脑水肿和心肌炎等,个别重型HFMD患儿病情进展快,易致死亡.HFMD发病机制可能与病毒感染所致免疫功能异常有关,尤其是细胞免疫功能低下.此外,EV71病毒感染导致的全身炎症反应综合征(SIRS)也可能参与HFMD的发病.因此早期对HFMD患儿进行细胞免疫支持治疗,并阻断SIRS发展,对改善预后意义重大.     

我国女性职业健康与职业发展之路——写在中国共产党建党100周年

儿童多系统炎症综合征（multisystem inflammatory syndrome in children, MIS-C）是一种以发热、消化道症状、心脏损害及休克等多系统受累为特征的疾病，伴炎症及心肌损伤标志物明显升高，同时存在严重急性呼吸综合征冠状病毒-2（severe acute respiratory syndrome-associated coronavirus, SARS-CoV-2）感染证据或2019新型冠状病毒病（coronavirus disease 2019, COVID-19）接触史。MIS-C的发病机制尚未明确，可能与SARS-CoV-2感染后继发的免疫失调有关，目前多在欧美国家报道。MIS-C与川崎病临床表现相似，主要不同是该病与SARS-CoV-2感染相关。60%的MIS-C患儿需要重症监护，大多接受抗炎和免疫调节为主的综合治疗，病死率为0.9%～2.0%。目前全球COVID-19疫情防控仍面临严峻挑战，儿科医生应提高识别MIS-C的能力。     

The potential role of HLA-G in the pathogenesis of HBV infection: Immunosuppressive or immunoprotective?

The non-classical human leukocyte antigens (HLA)-G could be generally considered as a potent tolerogenic molecule, which modulates immune responses. HLA-G due to the immunosuppressive properties may play an important role in the pathogenesis of infections related to the liver. HLA-G may display two distinct activities in the pathological conditions so that it could be protective in the autoimmune and inflammatory diseases or could be suppressive of the immune system in the infections or cancers. HLA-G might be used as a novel therapeutic target for liver diseases in the future. Indeed, new therapeutic agents targeting HLA-G expression or antibodies which block HLA-G activity are being developed and tested. However, further consideration of the HLA-G function in liver disease is required. This review aims to summarize the role of HLA-G in the liver of patients with HBV infection.     

The role of CCR5 in Chagas disease - a systematic review

Chagas disease is an infection caused by the protozoan Trypanosoma cruzi. The clinical manifestations result from the chronic forms of the disease: indeterminate, cardiac, digestive or mixed. The pathogenesis of this disease is related to the genetic variability of both the parasite and the host with polymorphisms of genes involved in immune response possibly being involved in the variable clinical course. Cytokines play a key role in regulating immune response, in particular chemokines exert a crucial role in the control of leukocyte migration during the host's response to infectious processes. Furthermore, inflammatory cytokines and chemokines have been implicated in the generation of inflammatory infiltrates and tissue damage. The involvement of the CC Chemokine Receptor 5 (CCR5) in leukocyte migration to sites of inflammation has been elucidated and this receptor has been investigated in Chagas disease. Here we review the role of CCR5 in T. cruzi infection as well as its importance in the pathogenesis of the Chagas disease.     

Is vaccination against transmissible spongiform encephalopathy feasible?

Prion diseases are a unique category of illness, affecting both animals and humans, where the underlying pathogenesis is related to a conformation change of the cellular form of a normal, self-protein called a prion protein (PrP(c) [C for cellular]) to a pathological and infectious conformation known as scrapie form (PrPsc [Sc for scrapie]). Currently, all prion diseases are without effective treatment and are universally fatal. The emergence of bovine spongiform encephalopathy and variant Creutzfeldt-Jakob disease has highlighted the need to develop possible therapies. In Alzheimer's disease (AD), which has similarities to prion diseases, both passive and active immunisation have been shown to be highly effective at preventing disease and cognitive deficits in model animals. In a human trial of active vaccination in AD, despite indications of cognitive benefits in patients with an adequate humoral response, 6% of patients developed significant complications related to excessive cell-mediated immunity. This experience highlights that immunotherapies designed to be directed against a self-antigen have to finely balance an effective humoral immune response with potential autoimmune toxicity. Many prion diseases have the gut as a portal of infectious agent entry. This makes mucosal immunisation a potentially very attractive method to partially or completely prevent prion entry across the gut barrier and to also produce a modulated immune response that is unlikely to be associated with any toxicity. The authors' recent results using an attenuated Salmonella vaccine strain expressing the prion protein show that mucosal vaccination can partially protect against prion infection from a peripheral source, suggesting the feasibility of this approach.     

Restricted leptin antagonism as a therapeutic approach to treatment of autoimmune diseases

Leptin, the adipocyte derived hormone, has a pivotal role in regulating energy homeostasis and appetite. Beyond this essential role in bodyweight control, leptin also regulates the immune responses. Leptin has pro-inflammatory effects on T cell populations, shifting the T helper balance towards a TH1 phenotype, through induction of pro-inflammatory cytokines and stimulation of macrophage and natural killer cell function. Acute starvation reduces serum leptin levels, resulting in an impaired cellular immune response. The TH1 pro-inflammatory immune response, a homeostatic response mediated by the low leptin levels, is also impaired during starvation. Leptin-deficient or leptin receptor mutant mice are protected against the development of several inflammatory or various T cell-dependent autoimmune diseases. Therefore, leptin appears to have a central role in the immune response and low leptin levels may protect against autoimmune disease. Here we review the role of leptin in the immune responses, with emphasis on autoimmune diseases. We will also discuss the application of leptin antagonist therapy for prevention and treatment of immunity related disorders.     

Longevity of Middle East Respiratory Syndrome Coronavirus Antibody Responses in Humans,Saudi Arabia

Understanding the immune response to Middle East respiratory syndrome coronavirus (MERS-CoV) is crucial for disease prevention and vaccine development. We studied the antibody responses in 48 human MERS-CoV infection survivors who had variable disease severity in Saudi Arabia. MERS-CoV–specific neutralizing antibodies were detected for 6 years postinfection.     

轮状病毒动物感染模型研究进展

建立动物模型对于疾病致病机理、疫苗研制、药物筛选都具有重要意义。疾病动物模型的建立不仅与病原体的特性有关,还涉及到动物的种类。至今,用于轮状病毒感染的动物模型尚且不多,具有敏感性又适用于大多数毒株的,能完全模拟人的致病过程的实验动物还不确定,给轮状病毒疫苗及治疗药物的研发带来了很大的不便。为推进寻求理想的轮状病毒实验动物模型,查阅近几年国内外关于轮状病毒感染动物模型种类、利用轮状病毒感染动物模型进行的相关实验研究进展以及相关的文献报道,并对其进行了总结分析,为将来可能的优化、选择轮状病毒感染动物模型提供理论参考依据。