乙型肝炎病人外周血树突状细胞亚群鉴定及其临床意义

近年来的研究认为,树突状细胞(DC)在人体免疫系统应答过程中发挥重要作用[1],根据其细胞表面标志不同,可将DC分为DC1和DC2亚群[2]。我们对慢性乙型肝炎病人外周血DC亚群变化及其功能与疾病的发生、发展等关系进行分析。资料与方法一、研究对象随机选择解放军第251医院2001年5月～10月住院慢性乙型肝炎病人24例(其中轻、中型19例,重型5例),男17例,女3例,平均年龄29.5(12～47)岁。诊断符合2000年9月全国第十次病毒性肝炎及肝病学术会议(西安)修订标准。全部病例排除其他型病毒性肝炎感染。对照者为10名健康自愿献血者,其中男8例,女2例,平…     

乙型肝炎患者免疫促进剂治疗前后T淋巴细胞亚群及NK细胞的…

对６２例慢乙肝患者Ｔ淋巴细胞亚群及ＮＫ细胞检测，并观察分别经ｉＲＮＡ、猪苓多糖及ＬＡＫ细胞治疗前后的细胞数量变化。结果发现治疗前ＣＤ＾＋４细胞降低，ＣＤ＾＋８细胞增高。ＣＤ＾＋４／ＣＤ＾＋８比值下降。治疗后ＣＤ＾＋４细胞及ＮＫ细胞增高，ＣＤ＾＋４／ＣＤ＾＋８比值上升，其中以ＬＡＫ细胞治疗效果显著，与ＨＢＶＭ转阴呈正相关。说明提高机体免疫功能对清除病毒有一定作用。     

Graves病患者外周血T细胞亚群和NK细胞活性的变化

我们以单克隆抗体技术检测了Graves病(GD)患者治疗前外周血T细胞亚群,以~(51)Cr释放法动态观察了患者在治疗不同时期NK细胞活性的变化,并探讨了GD与NK细胞功能的关系以及抗甲状腺药物对其的影响作用。     

检测慢性乙肝患者外周血T细胞亚群,NK细胞活性及sIL—2R的临床意义

我们对67例慢性乙肝患者进行外周血T淋巴细胞亚群、NK细胞活性与白细胞介素2受体(sIL—2R)检测,以探讨其与慢性乙肝病情演变及预后的关系。1 资料与方法1.1 一般资料 67例慢性乙肝患者,男41例,女26例,年龄20～57岁,平均42.3岁;病程2.5～15年,平均8.4年。慢迁肝(CPH)32例,慢活肝(CAH)25例,重肝(CFH)10例。67例均符合1990年第六届全国肝病会议(上海)制定的诊断标准。其中38例用促肝细胞生长素(100mg加入0.9％生理盐水静滴,1次/d)治疗3个月。另设     

老年肿瘤患者T淋巴细胞亚群和NK细胞数量的观察

老年肿瘤患者Ｔ淋巴细胞亚群和ＮＫ细胞数量的观察高秀子一、资料与方法１．研究对象：选自我院１９９３年至１９９７年经病理组织学（６５例）、Ｂ超（３例）、ＣＴ（８例）证实为肿瘤的老年患者７６例，其中肺癌１６例，结直肠癌１４例，胃癌１０例，肾癌、乳腺癌各８例...     

NKT细胞在肝脏疾病中的作用

自然杀伤T细胞(natllral killer T cells.NKT细胞)是一种同时具有NK细胞和T细胞部分表型及功能的细胞亚群.他能将先天性免疫应答和获得性免疫应答连接起来,限制性识别CDld-糖脂抗原、活化后迅速分泌大量细胞因子从而调节机体的免疫应答.人体的肝脏内富含NKT细胞,因此,NKT细胞在肝脏中的作用引起了人们的广泛兴趣.     

乙肝患者外周血B细胞和T细胞及其亚群的研究

应用免疫学技术对乙肝患者进行了外用血Ｂ细胞和Ｔ细胞及其亚群的测定，结果发现，乙肝患者Ｂ细胞明显高于正常人（Ｐ〈０．０１），ＯＫＴ３，ＯＫＴ４，ＯＫＴ４／ＯＫＴ８比值明显地低于正常人（Ｐ〈０．０１），ＯＫＴ８明显地高于人（Ｐ〈０．０１），说明乙肝患者是一种免疫调节异常的一种自身免疫性疾病。     

慢性胃炎,胃溃疡及胃癌患者外周血T细胞亚群及NK细胞的临床意义

慢性胃炎、胃溃疡及胃癌患者外周血Ｔ细胞亚群及ＮＫ细胞的临床意义王民登，王超（右江民族医学院附属医院内科）近年来免疫功能紊乱与胃病关系受到人们的重视。作者检测了１５７例胃病患者外周血Ｔ细胞亚群及自然杀伤细胞（ＮＫ细胞），以探讨其临床意义。材料和方法检测...     

急性和慢性乙型肝炎患者外周血NK细胞和T淋巴细胞亚群的动态变化

目的：观察急性和慢性乙型肝炎患者急性期和恢复期外周血NK细胞和T淋巴细胞亚群的变化。方法在40例急性乙型肝炎和40例慢性乙型肝炎患者,分别在急性期和恢复期检测CD3＋CD4＋T细胞、CD3＋CD8＋T细胞和NK（CD3-CD16＋CD56＋）细胞占淋巴细胞的比率（%）。结果在急性乙型肝炎急性期NK细胞计数为（15.7±7.5）%,而在恢复期则上升至（21.9±8.2）%,（P＜0.05）;急性乙型肝炎患者在急性期CD3＋CD4＋T细胞为（35.5±6.8）%,到恢复期则显著下降（33.6±7.0）%,（P＜0.05）;急性乙型肝炎在急性期CD3＋CD8＋T细胞为（35.6±7.6）%,而在恢复期则显著下降（30.0±7.5）%,（P＜0.05）,后者仍比慢性乙型肝炎患者在病情恢复期高（19.1±7.1）%,（P＜0.05）。结论在急性乙型肝炎病程中,NK细胞呈上升趋势,CD3＋CD8＋T细胞呈下降趋势,而在慢性乙型肝炎患者NK细胞及T淋巴细胞数量下降,致病情迁延不愈。     

Pivotal roles of the interleukin-23/T helper 17 cell axis in hepatitis B

T helper 17 (Th17) cells are a newly identified subset of T helper cells that play important roles in host defense against extracellular bacteria, as well as in the pathogenesis of autoimmune disease. Research interest in these cells was piqued when hepatitis B virus (HBV)-infected patients were found to have significantly elevated Th17 cell frequency, and it was proposed that these proinflammatory effectors may promote the HBV disease process. Subsequent studies have revealed that Th17 cells drive immune-mediated pathology of HBV infection, and that IL-23 amplifies the Th17 cell responses and liver inflammation. As a result, new pathways of HBV-mediated liver damage have been elucidated, along with promising new targets of molecular therapeutic strategies. Ongoing research is also providing significant insights into the target cells and underlying mechanisms of Th17-secreted cytokines, including IL-17A, IL-21 and IL-22. Future studies are expected to fully uncover the cytokine-related mechanisms mediating HBV-induced liver inflammation, and to determine the yet unknown cell source of IL-23. This review will draw upon the most up-to-date available data to discuss the putative roles and detailed mechanisms of IL-23/Th17 cell axis in HBV infection-mediated liver pathogenesis.     

HBV感染者自然杀伤细胞活性分析

目的 探讨不同临床病期的慢性HBV感染者外周血单个核细胞(PBMC)中T淋巴细胞亚群及NK细胞活性变化.方法 收集慢性乙型肝炎、慢性重型乙型肝炎、乙型肝炎肝硬化、肝癌四组患者及健康人群的外周血,应用流式细胞术检测CD8+T细胞、CD4+T细胞及NK细胞的表达量和分泌细胞因子的能力,并检测NK细胞的杀伤活性.结果 各组患...     

慢加急性乙型肝炎肝衰竭患者乙型肝炎病毒前C/CP区变异研究进展*

慢加急性肝衰竭（ACLF）是我国肝衰竭的主要类型,其病情发展迅速、预后不良、病死率较高。在我国,乙型肝炎病毒（HBV）感染是导致ACLF的主要病因,其中HBV前C（PC）/核心启动子（CP）区基因变异与ACLF的发生密切相关。本文重点介绍HBV PC/CP区基本结构和功能、PC/CP区变异后生物学特性的改变、ACLF的免疫病理损伤机制、PC/CP区变异与ACLF疾病进展的临床意义等方面的研究进展。     

乙型肝炎病毒蛋白结合蛋白的研究

0引言随着基因组测序工作的完成,后面就是研究基因的功能,其中基因表达蛋白质的功能的研究尤为重要,因为基因是通过蛋白质起作用的.蛋白质与蛋白质之间的相互作用揭示了蛋白质功能的物理基础之一,即蛋白质起作用是通过与另一蛋白质进行物理接触而完成.大家知道乙型肝炎病毒(HBV),对人体有着广泛的作用,如引起人免疫紊乱?慢性肝炎?肝硬化?肝肿瘤发生,治疗效果不佳[1-9],但是他们是如何作用的目前不是太清楚,但是可以肯定其中具有蛋白质-蛋白质之间的相互作用.1990年代以来一系列遗传?生化方法特别是酵母双杂交技术等进展,为研究HBV与人体…     

树突状细胞在乙型病毒性肝炎防治中的研究进展

我国是乙型肝炎病毒 (ＨＢＶ)感染的高发区 ,慢性乙型肝炎患者约 3千万 ,造成乙型肝炎慢性化的主要原因是ＨＢＶ感染所形成的免疫功能不全、体内高滴度病毒含量及对受染细胞的耐受状态 ,因此打破ＨＢＶ感染后的耐受状态是治疗慢性乙型肝炎的关键[1] 。抗原提呈细胞 (ＡＰＣ)是机体免疫反应的首要环节 ,能否进行有效的抗原提呈直接关系到免疫激活或免疫耐受的诱导。而树突状细胞 (ｄｅｎｄｒｉｔｉｃｃｅｌｌｓ ,ＤＣ)是功能强大的专职抗原提呈细胞 ,在免疫应答的诱导中具有特殊地位[2 ] 。目前 ,ＤＣ应用于乙型肝炎的预防和治疗已有了一定的…     

乙型肝炎病毒垂直传播机制的研究进展

垂直传播是乙型肝炎病毒(HBV)的主要传播途径之一。狭义的垂直传播,指患者的生殖细胞受病毒感染,在受精时由精子或卵细胞作为载体,将病毒基因带入胚胎进而使子代患病。迄今为止,文献中提到的垂直传播多指广义的垂直传播,即感染HBV的父亲和(或)母亲与婴儿之间,经生殖细胞、宫内感染、分娩及产后接触等途径所实现的HBV传播。     

NK and NKT cell dynamics after rituximab therapy for systemic lupus erythematosus and rheumatoid arthritis

Biomarkers of clinical response to rituximab (RTX) therapy and early predictors of outcome are still under investigation. We report a flow cytometric immunophenotyping analysis from peripheral blood leukocyte subpopulations of two patients with systemic lupus erythematosus (SLE) associated thrombocytopenia and one patient with rheumatoid arthritis (RA), before and after 6 weeks of treatment with RTX. Our results show a reduced population of CD19(+) expressing cells (B cells) after RTX treatment in all three patients. Increased frequency of peripheral regulatory CD4(+)CD25(high) T cell subset and the CD3(-)CD16(-)CD56(bright) NK cell subset after RTX therapy were also observed in all patients, the latter being more pronounced in the SLE patient with sustained clinical response. In addition, an increased population of NKT cell subsets was observed in the patients with clinical response. This is the first evaluation of NK and NKT cells as biomarkers of clinical response after rituximab therapy in rheumatic diseases.     

Invariant NKT cells sustain specific B cell responses and memory

Invariant natural killer T (iNKT) cells are innate-like lymphocytes recognizing CD1d-restricted glycolipid antigens, such as alpha-galactosylceramide (alphaGC). We assessed whether iNKT cells help B lymphocyte responses and found that mice immunized with proteins and alphaGC develop antibody titers 1-2 logs higher than those induced by proteins alone. Activation of iNKT cells enhances protection against infections such as influenza and elicits higher frequencies of memory B cells and higher antibody responses to booster immunizations. Protein vaccination with alphaGC, but not with conventional adjuvants, elicits IgG responses in mice lacking MHC class II molecules, demonstrating that iNKT cells can substitute for CD4(+) T cell help to B cells. Interestingly, the decay of circulating antibodies is faster in mice lacking iNKT cells. These findings point to a homeostatic role for iNKT cells on critical features of the antibody response such as immunity and B cell memory.     

Blockade of NKG2D on NKT cells prevents hepatitis and the acute immune response to hepatitis B virus

Hepatitis B virus (HBV) is a hepadnavirus that is a major cause of acute and chronic hepatitis in humans. Hepatitis B viral infection itself is noncytopathic, and it is the immune response to the viral antigens that is thought to be responsible for hepatic pathology. Previously, we developed a transgenic mouse model of primary HBV infection and demonstrated that the acute liver injury is mediated by nonclassical natural killer (NK)T cells, which are CD1d-restricted, but nonreactive to alpha-GalCer. We now demonstrate a role for NKG2D and its ligands in this nonclassical NKT cell-mediated immune response to hepatitis B virus and in the subsequent acute hepatitis that ensues. Surface expression of NKG2D and one of its ligands (retinoic acid early inducible-1 or RAE-1) are modulated in an HBV-dependent manner. Furthermore, blockade of an NKG2D-ligand interaction completely prevents the HBV- and CD1d-dependent, nonclassical NKT cell-mediated acute hepatitis and liver injury. This study has major implications for understanding activation of NKT cells and identifies a potential therapeutic target in treating hepatitis B viral infection.