The role of VCAM-l/VLA-4 in the activation of allogenic T cells by murine macrophages

Vascular cell adhesion molecule 1 (VCAM-1) is a member of immunoglobulin superfamily. The principal ligand for VCAM-1 is integrin α4β/VLA-4 (very late antigen 4). It was reported that VCAM-1 was expressed on macrophages and dendritic cells, but little is known about its function on these professional antigen presenting cells (APC). The present study was performed to investigate the expression of VCAM-1 on macrophages and the role of VCAM-l/VLA-4 in the activation of allogenic T cells by murine macrophages. We analyzed VCAM-1 expression on peritoneal macrophages and macrophage cell line J774A.1 by fluorescence-activated cell sorting (FACS). Using neutralizing antibodies, we further analyzed the role of VCAM-l/VLA-4 interaction in macrophage and allogenic T cell mixed lymphocyte reaction (MLR). We found that VCAM-1 was constitutively expressed on macrophages and its expression level was upregulated by soluble tumor associated antigen (freeze-thaw lysates of FBL-3 leukemia cells) and TNF-a. In MLR assays, we observed that blocking VCAM-l/VLA-4 interaction with anti-VCAM-1 or anti-VLA-4 mAbs caused significant inhibition of the proliferative response and IL-2 production. These results suggest that VCAM-lon macrophages not only facilitates the cell-to-cell contact through adhesive interaction but also plays a role in the costimulation of T cells via its interaction with VLA-4 on the T cells. This work was supported by grants from the National Natural Science Foundation of China.No. (39730420). This is one of papers of the special issue on gene therapy research (Chin J Cancer Res Vol. 9 No. 4 December, 1997).     

经IFN-γ诱导的人IL-2基因修饰的人原代成纤维细胞体外细胞因子表达及某些免疫学特性的研究

成纤维细胞作为基因治疗载体细胞是肿瘤基因治疗的一项重要途径,但以往的研究仅仅将成纤维细胞作为载体而忽略了其自身的免疫学功能的发挥。本文采用本室构建的逆转录病毒载体将IL-2基因转入人原代成纤维细胞,再用IFN-7诱导。结果表明,IFN-7诱导后,IL-2基因修饰的成纤维细胞MHC-Ⅰ、MHC-Ⅱ、CD40等分子表达具有一定程度的增高,并且表达IL-2、IL-1、IL-6等,由于这些免疫分子及细胞因子的表达与肿瘤抗原的递呈、效应细胞的激活密切相关,提示这种经IFN-7诱导后的IL-2基因修饰的成纤维细胞可能作为抗原递呈细胞而参与肿瘤抗原的递呈及效应细胞的激活。     

肿瘤患者合并肺部念珠菌感染药敏测定研究

采用ＲＰＭＩ１６４０及ＦＤＡ抗生素３号两种培养基的微量稀释法对肿瘤患者合并肺感染分离出５１株念珠菌进行药敏对比测定。结果显示二性霉素Ｂ在两种培养基中均具有非常好的抗菌活性，敏感率均为９８．０％，其次酮康唑也显示出良好的抗菌活性，敏感率均为９４．１％。相比之下，在ＲＰＭＩ培养基中伊曲康唑和氟康唑的敏感性稍差，敏感率分别为９２．２％和９０．２％，但在ＦＤＡ抗生素３号培养基中，伊曲康唑和氟康唑敏感性明显下降，敏感率分别为７０．６％和６６．７％。为此我们建议抗真菌药敏试验，尤其是咪唑类药物应该选用ＮＣＣＬＳ推荐的ＲＰＭＩ１６４０培养基做药敏试验     

NK细胞识别的新模式——压力诱导模式

T、B细胞通过TCR和BCR介导抗原识别模式,巨噬细胞通过模式识别受体(pattern recognition receptor,PRR)介导病原体相关的分子模式(pathogen associated molecular pattern, PAMP)或凋亡细胞相关的分子模式(apoptotic cell associated molecular pattern, ACAMP),比TCR,BCR和PRR更为复杂的是NK细胞的受体,迄今为止,已发现有数十种之多,分属抑制性受体和活化性受体两大类.各大类又包括数个家族,体现了NK细胞受体的多样性,介导了NK细胞的不同识别模式,分别传递不同的活化信号和抑制信号[1-2].     

我院麻醉药品及精神药品的用药分析

目的了解麻醉药品、精神药品的临床应用情况及用药趋势。方法统计分析我院药库微机管理系统提供的2002-2003年麻醉药品、精神药品的数据。结果2002-2003年我院麻醉药品、精神药品中美施康定片和安定片的用药频度都处于第1位,吗啡类制剂用量增幅较大。结论麻醉药品、精神药品作为特殊管理的药品,应加强药品管理和注意合理用药。     

艾滋病预防控制策略

1世界艾滋病预防控制的经验与措施自1981年在美国首次报告获得性免疫缺陷综合征(简称艾滋病, AIDS)临床患者至今已20多年, AIDS已蔓延至世界各地,成为人类面临的危害最大的疾病之一。目前,全球累计艾滋病病毒(H IV)感染者已超过7000万。世界卫生组织(WHO )和联合国艾滋病规划署(UN-AIDS)估计至2004年底全球存活的H IV /AIDS人数已达3940万(3590~4430万)。在艾滋病的预防控制工作中,世界各国积累了许多丰富的经验和有效的控制策略,其中有些具有基本的、普遍性的原则,我们可以学习借鉴。它们主要体现在以下几方面。1·1政府重视,经…     

Inducible nitric oxide synthase expression elicited in the mouse brain by inflammatory mediators circulating in the cerebrospinal fluid

Expression of inducible nitric oxide synthase (iNOS) protein was studied in the brain after intracerebroventricular injections of interferon (IFN)-gamma, and IFN-gamma combined with lipopolysaccharide (LPS) or tumor necrosis factor (TNF)-alpha, compared to ovalbumin as control. Wild-type mice and mice with targeted deletion of the IFN-gamma receptor gene were used. Findings based on iNOS immunoreactivity were evaluated at 1, 2, 4 and 7 days post-injection, using also quantitative image analysis and double labeling with glial cell markers. IFN-gamma administration induced iNOS immmunostaining in activated microglia and macrophages in the parenchyma surrounding the ventricular system, several cortical fields and fiber tracts. IFN-gamma-elicited iNOS immunoreactivity was down-regulated after 1 day. The number of iNOS-immunopositive cells was significantly enhanced by co-administration of LPS or TNF-alpha; IFN-gamma+TNF-alpha injections also resulted in longer persistence of iNOS immunoreactivity. No immunopositive cells were seen in the brain of IFN-gamma receptor knockout mice after IFN-gamma administration; very few immunostained macrophages were detected in these cases, mostly around the injection needle track, after co-administration of LPS or TNF-alpha. Western blot analysis confirmed a marked iNOS induction in the brain of wild-type mice 24 h after IFN-gamma+LPS injections. The findings show that inflammatory mediators circulating in the cerebrospinal fluid induce in vivo iNOS in the brain with topographical selectivity and temporal regulation. The data also demonstrate that the signaling cascade activated by IFN-gamma binding to its receptor is critical for iNOS induction, and the synergistic action of LPS and TNF-alpha as iNOS inducers in brain cells is largely mediated by the receptor-regulated action of IFN-gamma.     

尿激酶型纤溶酶原激活剂对大鼠面神经损伤修复的影响

目的 :探讨尿激酶型纤溶酶原激活剂 (uPA)在神经再生微环境中的作用机制 ,观察uPA对面神经断伤吻合后神经再生修复的影响。方法 :将 2 4只SD大鼠随机分为uPA组和对照组 ,建立大鼠面神经断伤修复模型 ,uPA组术后连续 5d腹部皮下注射uPA ,每天 3次 ,每次 5 0 0 0U/kg ,对照组注射等体积生理盐水。术后 1,7,14 ,2 1,4 2 ,84d取吻合处远侧段面神经 ,采用形态学、免疫组织化学和图像分析技术 ,观察分析两组中神经纤维的等效直径、周长和面积参数以及纤维连结蛋白 (fibronectin ,FN)和层粘连蛋白 (laminin ,LN)伤后早期的表达变化。结果 :术后 2 1,4 2d时uPA组新生神经纤维髓鞘面积和 4 2d时等效直径均较对照组恢复好 (P <0 .0 5 )。FN在术后表达逐渐增强 ,14 ,2 1d时较对照组明显增多 (P <0 .0 5 )。两组中LN术后表达均减少 ,随再生过程而逐渐增多 ,组间差别无统计学意义。结论 :面神经断伤吻合后应用uPA可降解纤维蛋白 ,使FN表达上调 ,有利于改善神经再生后的微环境 ,提高新生神经纤维的再生修复效果     

全麻下改良额肌瓣悬吊术治疗儿童先天性重度上睑下垂临床观察

目的寻找一种治疗先天性重度上睑下垂的有效手术方法。方法总结94眼先天性重度上睑下垂行改良额肌瓣悬吊术。结果94眼中85眼满意(90%),94眼基本满意(100%)。结论该术式简单,效果好,是治疗先天性重度上睑下垂的首选方法。     

表面麻醉下小梁切除术的临床观察

目的:探讨表面麻醉下小梁切除术的麻醉效果。方法:消毒前用表面麻醉药4g/L盐酸丁氧普鲁卡因点结膜囊内,2～3滴/次,放置开睑器前再点2次。用白内障超声乳化隧道刀、穿刺刀、侧切刀做常规小梁切除术。结果:术中无疼痛者29例(34眼);术中虹膜根切时轻度疼痛伴眼胀者5例(6眼);2例(2眼)缝合球结膜时痛疼明显但能耐受未予以追加麻醉。术后30min轻度眼胀眼痛不适者8眼,均未处理,1～2h后缓解。术后视力提高2行以上者34眼,8眼视力无变化。自动电脑视野计检查视野较术前扩大12眼,余30眼无明显视野继续损害。39眼眼压控制在1.20～2.40kPa,3眼眼压控制在2.67～3.33kPa。