FK506对人外周血T淋巴细胞CD28分子表达的体外…

应用淋巴本外化模型和流式细胞分析技术，观察异体角膜体外对人外周血Ｔ淋巴细胞ＣＤ２８分子表达的调节和ＦＫ５０６对Ｔ淋巴细胞ＣＤ２８表达的抑制作用，结果显示：空白对照组Ｔ淋巴细胞ＣＤ２８表达为２１．３％；受异体角膜或ＰＤＢ刺激后，Ｔ淋巴细胞ＣＤ２８表达分别为５２．４％和８１．４％，同时加入ＦＫ５０６的实验组，Ｔ淋巴细胞ＣＤ２８表达分别为２４．５％和４１．９％，结果表明异体角膜体外能够刺激Ｔ淋巴细胞ＣＤ     

FK506对人外周血T淋巴细胞CD_(28)分子表达的体外抑制作用

应用淋巴细胞体外活化模型和流式细胞分析技术，观察异体角膜体外对人外周血Ｔ淋巴细胞ＣＤ２８分子表达的调节和ＦＫ５０６对Ｔ淋巴细胞ＣＤ２８表达的抑制作用．结果显示：空白对照组Ｔ淋巴细胞ＣＤ２８表达为２１．３％；受异体角膜或ＰＤＢ刺激后，Ｔ淋巴细胞ＣＤ２８表达分别为５２．４％和８１．４％，同时加入ＦＫ５０６的实验组，Ｔ淋巴细胞ＣＤ２８表达分别为２４．５％和４１．９％·结果表明异体角膜体外能够刺激Ｔ淋巴细胞ＣＤ２８分子表达，ＦＫ５０６体外能够明显抑制Ｔ淋巴细胞ＣＤ２８分子表达和活化．     

早孕妇女蜕膜中淋巴细胞抗原的分析

检测早孕蜕膜中淋巴细胞抗原的表达。以几种抗淋巴细胞表面标志的单克隆抗体,采用花环标记、碱磷酶抗碱磷酶（ＡＰＡＡＰ）法,对２３例早孕蜕膜组织中的淋巴细胞进行测定。早孕蜕膜淋巴细胞中ＣＤ３＋、ＣＤ４＋、ＣＤ１６＋及Ｂ细胞百分率（ｘ±ｓ）分别为２９．５２±６．８０％、２３．６０±４．８０％、２０．９１±４．０６％、１．０７±１．００％、７．８１±２．５６％,ＣＤ４／ＣＤ８为１．２±０．２,ＣＤ３－淋巴细胞呈大颗粒淋巴细胞（ＬＧＬ）形态。早孕蜕膜中存在较多ＣＤ３－、ＣＤ１６－形态呈ＬＧＬ的ＮＫ细胞,ＣＤ４＋细胞与ＣＤ８＋细胞的比值较正常外周血明显降低。     

半导体激光(650 nm,5 mW)血管内照射对人外周血淋巴细胞凋亡的影响

报道了用半导体激光进行血管内照射（ＩＬＩＢ）治疗１３例患者外周血淋巴细胞凋亡的影响．发现照射前ＰＣＤ为（５．４７±３．６５）％，第一次照射后为（７．１±３．１６）％，第五次照射后为（１６．７１±９．５）％．两者均有非常显著性差异（Ｐ＜０．０１）．     

阳离子对猪心细胞色素C的反胶团萃取的影响

在猪心提取液中添加阳离子的情况下，观察了ＡＯＴ／异辛烷反胶团对蛋白质和细胞色素Ｃ的萃取效果。结果表明：萃取分相以添加Ｍｇ（２＋）最好，其次分别为Ｎａ＋．Ｋ＋、Ｃａ（２＋）。在添加Ｍｇ（２＋）、Ｎａ＋，Ｃａ（２＋），Ｋ＋离子后，对蛋白质的萃取率分别为：５０．４％、３１．５％、２９．２％、２７．８％。在添加Ｍｇ（２＋），Ｎａ＋Ｋ＋离子时，对细胞色素的萃取率（以反萃取率表示）分别为４０．６％、３７．４％、＋３０．４％。     

急性心肌梗死患者外周血T淋巴细胞和NK细胞的 …

目的：研究急性心肌梗死患者外周血Ｔ淋巴细胞的变化。方法：采用流式细胞仪技术,观察１５例急性心肌梗死患者外周血Ｔ淋巴细胞ＣＤ２、ＣＤ３＾＋、ＣＤ４＾＋、ＣＤ８＾＋、ＣＤ１６＾＋、ＣＤ２５＾＋、ＣＤ２７＾＋、ＣＤ５７＾＋变化,并与１２例正常对照组比较,结果：ＣＤ２＾＋、ＣＤ３＾＋、ＣＤ１６＾＋、ＣＤ２７＾２＋、ＣＤ５７＾＋无显著性变化;ＣＤ４＾＋明显减少,ＣＤ８＾＋明显增加,ＣＤ４＾＋／ＣＤ８＾＋幽会     

添加剂对废水中COD,N和P去除的影响

实验室规模的ＡＮＡＮＯＸ工艺（ＡＮａｅｒｏｂｉｃ－ＡＮｏｘｉｃ－ＯＸｉｃ）用来处理豆制品废水，阐明添加剂对此工艺去除ＣＯＤ、Ｎ和Ｐ能力．研究结果表明：ＴＣＯＤ去除９５．７％，ＳＣＯＤ去除９５．８％，去除９４．２％，去除８９．１％，ＴＫＮ去除８２．４％，ＴＰ去除８７．４％，ＳＰ去除７７．２％，ＳＳ去除９８．０％．比加添加剂之前去除率提高了ＴＣＯＤ９．９％，ＳＣＯＤ１０．３％，ＴＰ４１．４％，ＳＰ３０．８％，ＳＳ８．１％     

化学沉积Ni-Cu-P合金及晶化处理对镀层结构和硬度的影响

从弱碱性化学镀溶液中化学沉积Ｎｉ－Ｃｕ－Ｐ合金,并用差热分析（ＤＳＣ）、Ｘ－射线衍射（ＸＲＤ）和透射电镜（ＴＥＭ）研究了晶化处理对镀层结构及硬度的影响。结果表明,镀液中ＣｕＳＯ４．５Ｈ２Ｏ浓度对合金组成有显著影响。在化学沉积过程中,Ｃｕ的优先析出使镀层中Ｃｕ／Ｎｉ摩尔比远远高于镀液中Ｃｕ＾２＋／Ｎ＾２＋摩尔比。镀液中ＳｕＳＯ４．５Ｈ２Ｏ浓度低时,沉积速度随其浓度增加而增大,但ＣｕＳＯ４．５Ｈ２Ｏ浓     

半导体激光（650nm,5mW）血管内照射对人外周血淋巴细胞凋亡…

报道了用半导体激光进行血管内照射（ＩＬＩＢ）治疗１３例患者外周血淋巴细胞凋亡的影响。发现照射前ＰＣＤ为（５．４７±３．６５）％，第一镒照射后为（７．１±３．１６）％，第五次辐射后为（１６．７１±９．５）％。两者均有非常显著性差异（Ｐ〈０．０１）。     

一种新的生物效应调节剂──PSP──ⅡPSP的临床学研究

本文报道了ＰＳＰ对４８５例肿瘤患者的巨期临床研究结果，采用随机、双盲法观察了服用ＰＳＰ患者在神疲乏力、食欲不振、口干咽燥、疼痛等临床证候上的效果，结果ＰＳＰ组有明显改善．用Ｋａｒｎｏｆｓｋｙ评分及疗前疗后体重法考察ＰＳＰ对肿瘤患者的生存质量，结果其增加例或稳定例明显高于对照组．测定肿瘤患者治疗前后的ＮＫ细胞活性、ＩＬ－２量及ＣＤ＋４／ＣＤ＋８值，结果ＰＳＰ组疗后的ＮＫ细胞活性上升例、ＩＬ－２增加例及ＣＤ＋４／ＣＤ＋８才提高例均比对照组有明显增加，表明ＰＳＰ能桔抗化疗或放疗引起的免疫抑制，测定ＰＳＰ对化疗或放疗患者的血象变化，无论其白细胞、血红蛋白或血小板数均与阳性对照组相仿，提示ＰＳＰ和阳性药一样，对血象有一定的保护效应．     

北五味子木脂素对酒精性肝损伤小鼠免疫功能的影响

目的观察五味子木脂素对小鼠淋巴细胞亚群和自然杀伤细胞(NK细胞)的影响.方法应用五味子木脂素高、中、低3个剂量治疗酒精性肝损伤小鼠,联苯双酯对照,观察其对小鼠脏器系数、体液免疫功能、淋巴细胞增殖以及NK细胞活性的影响,利用流式细胞仪和MTT法检测其对淋巴细胞亚群、NK细胞的影响.结果五味子木脂素中剂量组胸腺、脾脏系数明显增加,与对照组比较差异具有统计学意义(P0.05);五味子木脂素中剂量组能显著降低CD8+水平,提高CD3+,CD4+水平及CD4+/CD8+比值,与对照组比较差异具有统计学意义(P0.05);五味子木脂素中剂量能提高NK细胞活性和T,B淋巴细胞增殖能力,与对照组比较差异具有统计学意义(P0.05).结论五味子木脂素能够增强酒精性肝脏损伤小鼠的免疫功能.     

总状蕨藻盾叶变种多糖对小鼠T细胞亚群及NK细胞免疫功能的调节

目的:观察总状蕨藻盾叶变种多糖对正常小鼠T细胞亚群及NK细胞的免疫调节作用.方法:腹腔注射总状蕨藻盾叶变种多糖溶液,用流式细胞仪检测血中免疫参数(CD3 ,CD4 ,CD8 T细胞亚群百分比)和脾脏NK细胞百分比,并测定胸腺、脾脏指数.结果:总状蕨藻盾叶变种多糖能明显降低小鼠血中CD3 ,CD4 ,CD8 百分比(P＜0.05),同时增强脾脏NK细胞百分比(P＜0.05),并显著降低胸腺指数(P＜0.05),增加脾脏指数(P＜0.05).结论:总状蕨藻盾叶变种多糖对小鼠T细胞亚群和NK细胞具有双向的免疫调节作用.     

肺癌患者放疗前后外周血淋巴细胞亚群变化研究

目的探讨肺癌患者放化疗前后外周血淋巴细胞亚群的变化.方法应用流式细胞仪对30例健康正常人群(对照组)和68例肺癌患者(肺癌组)放化疗前后的外周血T淋巴细胞亚群、B淋巴细胞及NK细胞等进行检测,并比较分析健康人群和肺癌患者的变化情况.结果肺癌组放疗前外周血中CD3~+,CD4~+,CD4~+/CD8~+,CD19~+与对照组相比均有所下降,差异均具有统计学意义(P0.05);CD8~+比例较对照组升高,且差异具有统计学意义(P0.05);而CD56~+比例较对照组升高,但结果无统计学意义(P0.05).肺癌患者放化疗后淋巴细胞亚群CD3~+降低,CD56~+有所升高,差异无统计学意义(P0.05);CD4~+,CD4~+/CD8~+较治疗前降低,CD8~+,CD19~+较治疗前升高,差异均具有统计学意义(P0.05).结论肺癌患者在疾病发生、发展过程中存在淋巴细胞免疫异常和免疫功能紊乱的现象,外周血T,B淋巴细胞及NK细胞的检测对判断患者的免疫功能有一定参考作用.     

2型糖尿病患者神经-内分泌-免疫网络有关指标的紊乱及其临床意义

 为分析2型糖尿病患者神经-内分泌-免疫网络紊乱情况及其临床意义，选择174例经临床诊断明确的2型糖尿病患者，用放射免疫法和流式细胞技术检测外周血中CD4+、CD8+、NK细胞数量、CD4+/CD8+比值及IL-1β、IL-6、TNF-α、ACTH、CORT、DA、NE水平，选择30例健康志愿者为正常对照组进行相同检测。结果显示，与正常对照相比，2型糖尿病患者CD4+、CD8+及NK细胞数量下降（P<0.01），CD8+及CD4+/CD8+比值升高（P<0.01），IL-1β、IL-6和TNF-α均有升高（P<0.01），ACTH及CORT下降（P<0.01），DA和NE升高（P<0.01）。研究表明，2型糖尿病患者神经-内分泌-免疫网络的紊乱中，其体液免疫增强、细胞免疫减弱，交感神经兴奋及应激性内分泌功能减弱为主要表现。对于2型糖尿病的治疗，除采用现有手段，应加强机体对胰岛素抵抗调控平衡态的修复与重建，重视神经-内分泌-免疫系统标志的检测及相应的新治疗研究。     

太极拳锻炼对免疫平衡影响及其机制研究进展

通过整理与分析国内外文献,分析了太极拳锻炼影响CD4+/CD8+细胞平衡与T1/T2平衡的作用与机制.研究认为,太极拳锻炼可引起CD4+细胞数量与CD4+/CD8+细胞比值升高,该变化可能与MDC数量的增高促进了Th细胞的分化过程有关;太极拳锻炼可提升Th1细胞数量与Th1/Th2细胞比例以及Ⅰ型细胞因子IFN-γ,IL-2含量与IFN-γ/IL-4比值,诱发T1/T2平衡向T1方向漂移.该变化的机制可能是Treg数量的增高抑制了Th细胞的分化过程,从而降低了IL-4对Th1细胞分化的交互抑制作用.     

Engagement of the CD4 molecule influences cell surface expression of the T-cell receptor on thymocytes

The intrathymic differentiation process by which precursor cells derived from the bone marrow develop into immuno-competent T lymphocytes is poorly understood. Most thymocytes express both CD4 and CD8 accessory molecules, yet little is known about either the function of these molecules or the responsiveness of the CD4+8+ double positive thymocytes that bear them. Here, we address the possibility that CD4 engagement influences T-cell receptor (TCR) expression on developing thymocytes. We engaged CD4 molecules on murine thymocytes by in vivo injection of an anti-CD4 monoclonal antibody, which reduced the surface expression of CD4 on CD4+ thymocytes. More importantly, CD4 engagement also affected TCR expression on CD4+ thymocytes, but the effect on CD4+8+ double positive and CD4+8- single positive thymocytes was very different. CD4+8+ thymocytes responded to CD4 engagement by dramatically increasing surface expression of TCR, whereas CD4+8- thymocytes decreased surface expression of TCR. These results demonstrate that the effect of CD4 engagement on TCR expression is dependent upon the developmental state of the responding thymocyte, and, most interestingly, results in increased TCR expression by double positive thymocytes.     

CD4+ murine T cells develop from CD8+ precursors in vivo

The adult murine thymus contains four subpopulations of thymocytes defined by the T-cell surface antigens CD4 (L3T4) (a marker of helper T cells) and CD8 (Lyt2) (a marker of cytotoxic/suppressor T cells): CD4+8- and CD4-8+ (single positives), CD4+8+ (double positives) and CD4-8- (double negatives). To understand how T cells develop in the thymus, it is important to determine the lineage relationships among these subpopulations. In particular, the status of double positives, which make up approximately 80% of the total thymocyte population, has long been controversial. Some purpose that double positives are 'dead-end cells' that all die in the thymus, perhaps because they have been rejected by some selection process. Others suggest that, although most double positives die in the thymus, some develop into the more mature single positives that leave the thymus. The experiments presented here show that repeated injections of anti-CD8 monoclonal antibodies block the development of CD4+ cells, demonstrating that these cells develop from CD8+ precursors, probably double positive thymocytes, in vivo.     

Rae1 and H60 ligands of the NKG2D receptor stimulate tumour immunity

Natural killer (NK) cells attack many tumour cell lines, and are thought to have a critical role in anti-tumour immunity; however, the interaction between NK cells and tumour targets is poorly understood. The stimulatory lectin-like NKG2D receptor is expressed by NK cells, activated CD8+ T cells and by activated macrophages in mice. Several distinct cell-surface ligands that are related to class I major histocompatibility complex molecules have been identified, some of which are expressed at high levels by tumour cells but not by normal cells in adults. However, no direct evidence links the expression of these 'induced self' ligands with tumour cell rejection. Here we demonstrate that ectopic expression of the murine NKG2D ligands Rae1beta or H60 in several tumour cell lines results in potent rejection of the tumour cells by syngeneic mice. Rejection is mediated by NK cells and/or CD8+ T cells. The ligand-expressing tumour cells induce potent priming of cytotoxic T cells and sensitization of NK cells in vivo. Mice that are exposed to live or irradiated tumour cells expressing Rae1 or H60 are specifically immune to subsequent challenge with tumour cells that lack NKG2D ligands, suggesting application of the ligands in the design of tumour vaccines.     

Signal for T-cell differentiation to a CD4 cell lineage is delivered by CD4 transmembrane region and/or cytoplasmic tail.

Mature T cells express either CD4 or CD8 on their surface. Most helper T cells express CD4, which binds to class II major histocompatibility complex (MHC) proteins, and most cytotoxic T cells express CD8, which binds to class I MHC proteins. In the thymus, mature CD4+CD8- and CD4-CD8+ T cells expressing alpha beta T-cell antigen receptors (TCR) develop from immature thymocytes through CD4+CD8+ alpha beta TCR+ intermediates. Experiments using mice transgenic for alpha beta TCR suggest that the specificity of the TCR determines the CD4/CD8 phenotype of mature T cells. These results, however, do not indicate how a T cell differentiates into the CD4 or CD8 lineage. Here we show that the CD4 transmembrane region and/or cytoplasmic tail mediates the delivery of a specific signal that directs differentiation of T cells to a CD4 lineage. We generated transgenic mice expressing a hybrid molecule composed of the CD8 alpha extracellular domains linked to the CD4 transmembrane region and cytoplasmic tail. We predicted that this hybrid molecule would bind to class I MHC proteins through the extracellular domains but deliver the intracellular signals characteristic of CD4. By crossing our transgenic mice with mice expressing a transgenic alpha beta TCR specific for a particular antigen plus class I MHC protein, we were able to express the hybrid molecule in developing thymocytes expressing the class I MHC-restricted TCR. Our results show that the signal transduced by the hybrid molecule results in the differentiation of immature thymocytes expressing a class I-restricted TCR into mature T cells expressing CD4.