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背景与目的CIK细胞是过继免疫治疗的重要手段之一,简化体外培养过程从而提高其增殖率和杀瘤活性仍是目前研究的一个热点课题。本研究观察重组人纤维连接蛋白（recombinant human fibronectin,RN）诱导CIK细胞的生物学特性,建立一种高效、简便的体外CIK细胞扩增方法。方法抽取10名健康人外周静脉血各50mL,用淋巴细胞分离液分离单个核细胞,分别采用RN诱导法和传统方法培养CIK细胞,记录细胞增殖数;用流式细胞术测定免疫细胞表型和分泌IFN-γ、IL-4、穿孔素和颗粒酶B细胞的百分比;用MTT法测定CIK细胞对4种人肺癌细胞株的体外杀伤率。结果RN诱导的CIK细胞扩增倍数为传统方法的2.0倍-3.5倍,具有统计学差异（P〈0.05）;RN诱导组和传统方法组CD3＋CD16＋CD56＋细胞绝对数分别增加了3778倍和2069倍;RN诱导组细胞中CD3＋CD8＋细胞比例明显高于传统方法组（P〈0.05）;但CD3＋CD4＋细胞比例无统计学差异（P〉0.05）;对4种肺癌细胞株的体外杀伤活性无统计学差异（P〉0.05）。RN诱导的CIK较诱导前：分泌IFN-γ的细胞比例明显增加;分泌IL-4的细胞比例略有降低;释放穿孔素、颗粒酶B的阳性细胞比例较诱导前增加。结论RN诱导法是一种高效、简便的体外扩增CIK方法,可以替代传统方法。

目的探讨不同类型冠心病患者外周血辅助性T细胞亚群17（Th17）的变化及临床意义。方法选取20例急性心肌梗死（AMI）患者、23例不稳定性心绞痛（UA）患者、19例稳定性心绞痛（SA）患者,另选22例同期住院的非冠心病患者作为对照组。采用流式细胞术检测外周血Th17细胞的百分率;实时定量PCR检测相关基因IL-17A、RORγt和STAT3 mRNA的表达;ELISA法检测血浆IL-17A的浓度。结果①UA患者和AMI患者外周血中Th17细胞的百分率显著高于SA患者和对照组（P〈0.01）;②与SA组患者和对照组相比,UA组和AMI组患者Th17细胞相关基因IL-17A、RORγt和STAT3的mRNA表达显著增高或有增高趋势。结论 UA患者和AMI患者外周血中Th17细胞激活,Th17激活可能与斑块的不稳定密切相关

目的观察头孢地嗪对免疫性肝损伤小鼠外周血T细胞亚群的调节作用。方法采用卡介苗联合脂多糖诱导法建立免疫性肝损伤的小鼠模型；将造模成功的免疫性肝损伤小鼠随机分为胸腺肽组、头孢地嗪大、中、小剂量组、头孢曲松组和生理盐水组，连续给药7d，同时以正常小鼠作为对照组；采用免疫荧光染色技术，经流式细胞仪对小鼠的外周血T细胞亚群进行检测。结杲免疫性肝损伤合并败血症小鼠的CD3^＋（％）、CD4^＋（％）和CD8^＋（％）均明显低于正常小鼠，而头孢地嗪可有效地提高免疫性肝损伤合并败血症小鼠的CD3^＋（％）、CD4^＋（％）和CD4^＋／CD8^＋。结论头孢地嗪可通过调整CD4^＋和CD8^＋之间的平衡，有效地提高机体的免疫功能。

目的 探讨辅助性T细胞Th1和Th2细胞因子对肺癌患者的临床意义．为肿瘤的免疫治疗提供依据。方法 采用放射免疫(RIA)和酶联免疫吸附法(ELISA)检测86例肺癌患者、59例肺良性病患者及45例正常对照辅助性T细胞分泌的细胞因子。以IL-2和TNF-a的水平代表Th1型细胞因子．IL-4、IL-6和IL-8的水平代表Th2型细胞因子。结果 肺癌患者IL-2[(24.6士12.0)ug／L]的水平显著低于肺良性病患者[(71.1士25.4)ug／L](t=3.82，P<0.01)和正常对照[(69.3士19.5)ug／L](t=2.76，P<0.01)·IL-6[(0.13±0.04)ug／L]的水平显著低于正常对照[(0.23±0.05)ug／L)(t=3.39，P<0.01)，IL-4[(254.2±78.0)ug/L]、IL-8[(0.49±0.16)ug／L]、TNF-a[(2.76±1.12)ug／L]的水平明显高于肺良性病患者：(63.6±18.6)ug／L，(0.36±0.18)ug／L，(0.96士0.20)ug／L]及正常对照[(60.9±19.6)ug/L，(0.35士0.07)ug／L·(0.93士0.19)ug／L](t值分别为4.10、4.89和3.76．P均<0.01)，肺良性病患者和正常对照之间的IL-2、TNF-a、IL-4、IL-8均未见明显差异(P>0.05)，肺癌组IL-6的水平与肺良性病组[(0.15土0.04)ug／L]无明显差异(P>0.05)，肺良性病组IL-6的水平与正常对照组[(0.23士0.05)ug／L]有明显差异(P<0.05)。肺癌患者不同组织类型间及不同TNM分期间细胞因子比较无显著性差异(P>0.05)。结论 肺癌患者机体T辅助细胞Th1／Th2细胞因子失衡，可能在肺癌的发病机理中起着某种作用。通过纠正这些免疫失常可能成为肺癌治疗的重要手段。

R735.705

Natural killer T （NKT） cells are innate-like lymphocytes that generally recognize lipid antigens and are enriched in microvascular compartments of the liver. NKT cells can be activated by self- or microbial-lipid antigens and by signaling through toll-like receptors. Following activation, NKT cells rapidly secrete pro-inflammatory or anti- inflammatory cytokines and chemokines, and thereby determine the milieu for subsequent immunity or tolerance. It is becoming clear that two different subsets of NKT cells-type I and type II--have different modes of antigen recognition and have opposing roles in inflammatory liver diseases. Here we focus mainly on the roles of both NKT cell subsets in the maintenance of immune tolerance and inflammatory diseases in liver. Furthermore, how the differential activation of type I and type II NKT cells influences other innate cells and adaptive immune cells to result in important consequences for tissue integrity is discussed. It is crucial that better reagents, including CDld tetramers, be used in clinical studies to define the roles of NKT cells in liver diseases in patients.

Liver disease encompasses a wide variety of liver conditions, including liver failure, liver cirrhosis and a spectrum of acute and chronic hepatitis, such as alcoholic, fatty, drug, viral and chronic hepatitis. Liver injury is a primary causative factor in liver disease; generally, these factors include direct liver damage and immune-mediated liver injury. Neutrophils （also known as neutrophilic granulocytes or polymorphonuclear leukocytes （PMNs）） are the most abundant circulating white blood cell type in humans, and PMNs are a major innate immune cell subset. Inappropriate activation and homing of neutrophils to the microvasculature contributes to the pathological manifestations of many types of liver disease. This review summarizes novel concepts of neutrophil-mediated liver iniurv that are based on current clinical and animal model studies.

To better elucidate epigenetic mechanisms that correlate with the dynamic gene expression program observed upon T-cell differentiation, we investigated the genomic landscape of histone modifications in naive and memory CD8＋ T cells. Using a ChlP-Seq approach coupled with global gene expression profiling, we generated genome-wide histone H3 lysine 4 （H3K4me3） and H3 lysine 27 （H3K27me3） trimethylation maps in naive, T memory stem cells, central memory cells, and effector memory cells in order to gain insight into how histone architecture is remodeled during T cell differentiation. We show that H3K4me3 histone modifications are associated with activation of genes, while H3K27me3 is negatively correlated with gene expression at canonical loci and enhancers associated with T-cell metabolism, effector function, and memory. Our results also reveal histone modifications and gene expression signatures that distinguish the recently identified T memory stem cells from other CD8＋ T-cell subsets. Taken together, our results suggest that CD8＋ lymphocytes undergo chromatin remodeling in a progressive fashion. These findings have major implications for our understanding of peripheral T-cell ontogeny and the formation of immunological memory.

Although B cells play important roles in the humoral immune response and the regulation of adaptive immunity, B cell subpopulations with unique phenotypes, particularly those with non-classical immune functions, should be further investigated. By challenging mice with Listeria monocytogenes, Escherichia coli, vesicular stomatitis virus and Toll-like receptor ligands, we identified an inducible CDlla^hi FcγRIII^hi B cell subpopulation that is significantly expanded and produces high levels of IFN-γ during the early stage of the immune response. This subpopulation of B cells can promote macrophage activation via generating IFN-γ, thereby facilitating the innate immune response against intracellular bacterial infection. As this new subpopulation is of B cell origin and exhibits the phenotypic characteristics of B cells, we designated these cells as IFN-γ-producing innate B cells. Dendritic cells were essential for the inducible generation of these innate B cells from the follicular B cells via CD40L-CD40 ligation. Increased Bruton＇s tyrosine kinase activation was found to be responsible for the increased activation of non-canonical NF-κB pathway in these innate B cells after CD40 ligation, with the consequent induction of additional IFN-γ production. The identification of this new population of innate B cells may contribute to a better understanding of B cell functions in anti-infection immune responses and immune regulation.

The mucosal immune system defends against a vast array of pathogens, yet it exhibits limited responses to commensal microorganisms under healthy conditions. The oral-pharyngeal cavity, the gateway for both the gastrointestinal and respiratory tracts, is composed of complex anatomical structures and is constantly challenged by antigens from air and food. The mucosal immune system of the oral-pharyngeal cavity must prevent pathogen entry while maintaining immune homeostasis, which is achieved via a range of mechanisms that are similar or different to those utilized by the gastrointestinal immune system. In this review, we summarize the features of the mucosal immune system,focusing on T cell subsets and their functions. We also discuss our current understanding of the oral-pharyngeal mucosal immune system.