细胞间黏附分子1与移植肾急性排斥反应

目的:检测移植肾组织内细胞间黏附分子1的表达水平,分析其与移植肾急性排斥反应的关系.方法:选择解放军南京军区福州总医院全军器官移植研究所在2002/2005进行的72例尸体肾移植的移植肾穿刺活检标本72份,其中移植肾急性排斥反应54份,环孢素A中毒标本18份;并取8份正常肾组织作对照.采用免疫组化技术检测细胞间黏附分子1在移植肾内的表达,分析其与病理形态结构的关系.结果:发生急性排斥反应的受者肾小管上皮细胞间黏附分子1表达显著高于正常者及环孢素A中毒受者(P<0.05),且随移植肾排斥程度加重,细胞间黏附分子1表达明显增多(P<0.05).结论:细胞间黏附分子1的表达与移植肾急性排斥反应病理分级密切相关,移植肾组织内细胞间黏附分子1的检测对于肾移植后急性排斥反应的诊断具有参考价值.     

Intercellular adhesion molecule-1 is upregulated on peripheral blood T lymphocyte subsets in dual asthmatic responders.

To examine the role of adhesion molecules in T cell recruitment and activation during allergen-induced late asthmatic response (LAR), we evaluated the expression of lymphocyte function-associated antigen-1 alpha (LFA-1 alpha) and intercellular adhesion molecule-1 (ICAM-1) on peripheral blood T lymphocyte subsets from atopic asthmatic patients and their changes following allergen inhalation challenge. 12 atopic asthmatic patients were studied. Six patients showed only a single early response after allergen challenge, and six developed a dual response. At baseline, dual responders (DR) had a significantly higher expression of ICAM-1 on CD4+ and CD8+ T lymphocytes as compared with both single early responders (P < 0.005 and P < 0.02, respectively) and controls (P < 0.001, both comparisons). Allergen challenge was followed by a decrease of CD8+ ICAM-1+ T lymphocytes in all DR (P < 0.05) and of CD4+ ICAM-1+ T lymphocytes in four out of six DR, at the time of the LAR. At the same time, a significant rise in serum levels of the soluble form of ICAM-1 was observed in DR. These results suggest that peripheral blood immunoregulatory T lymphocytes are in a higher state of activation in DR as compared with early responders. The upregulation of ICAM-1 on these cells may be important in enhancing airway inflammation in patients with LAR.     

Intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 are increased in the plasma of children with sepsis-induced multiple organ failure

OBJECTIVES: To determine concentrations of circulating adhesion molecules endothelial (E)-selectin, intercellular adhesion molecule (ICAM)-1, and vascular cell adhesion molecule (VCAM)-1 in children with sepsis-induced multiple organ failure (MOF), and to determine associations among increased concentrations of these circulating adhesion molecules and important outcome measures. DESIGN: Prospective study. SETTING: University pediatric intensive care unit. PATIENTS: A total of 77 consecutive children with sepsis and 14 acutely ill children without sepsis. INTERVENTIONS: Plasma E-selectin, ICAM-1, and VCAM-1 concentrations and organ failure index (indicating number of failed organ systems) were determined in 77 children on days 1 and 3 of sepsis, and in 14 control children on pediatric intensive care unit day 1. Multivariate logistic regression analysis was used to determine associations between adhesion molecule concentrations and clinically relevant outcome measures. MEASUREMENTS AND RESULTS: Plasma concentrations of E-selectin, ICAM-1, and VCAM-1 were increased in children with sepsis vs. control on day 1 (p < .05). Plasma VCAM-1 (but not ICAM-1 or E-selectin) was increased in children with more than three organ failures vs. children with less than three organ failures (p < .05). Plasma ICAM-1 and VCAM-1 (but not E-selectin) concentrations independently predicted number of organs failed and development of more than three organ failures. Plasma ICAM-1 and VCAM-1 also predicted mortality and development of sequential (pulmonary/hepatic/renal) MOF (p < .05). CONCLUSIONS: The pronounced and persistent increase in plasma VCAM-1 and ICAM-1 that occurs in children with sepsis and persistent MOF may indicate a phenotypic change in endothelium toward a more proinflammatory state. Alternatively, the source for these adhesion molecules may be activated leukocytes and other cell types. Future studies are required to determine the role of ICAM-1 and VCAM-1 in the pathogenesis of sepsis-induced MOF.     

Intercellular adhesion molecule-1-deficient mice are protected against ischemic renal injury.

Studies in the rat have pointed to a role for intercellular adhesion molecule-1 (ICAM-1) in the pathogenesis of acute tubular necrosis. These studies used antibodies, which may have nonspecific effects. We report that renal ICAM-1 mRNA levels and systemic levels of the cytokines IL-1 and TNF-alpha increase 1 h after ischemia/ reperfusion in the mouse. We sought direct proof for a critical role for ICAM-1 in the pathophysiology of ischemic renal failure using mutant mice genetically deficient in ICAM-1. ICAM-1 is undetectable in mutant mice in contrast with normal mice, in which ICAM-1 is prominent in the endothelium of the vasa recta. Mutant mice are protected from acute renal ischemic injury as judged by serum creatinine, renal histology, and animal survival . Renal leukocyte infiltration, quantitated morphologically and by measuring tissue myeloperoxidase, was markedly less in ICAM-1-deficient than control mice. To evaluate whether prevention of neutrophil infiltration could be responsible for the protection observed in the mutant mice, we treated normal mice with antineutrophil serum to reduce absolute neutrophil counts to < 100 cells/mm3. These neutrophil-depleted animals were protected against ischemic renal failure. Anti-1CAm-1 antibody protected normal mice against renal ischemic injury but did not provide additional protection to neutrophil-depleted animals. Thus, ICAM-1 is a key mediator of ischemic acute renal failure likely acting via potentiation of neutrophilendothelial interactions.     

Intercellular adhesion molecule 3, a third adhesion counter-receptor for lymphocyte function-associated molecule 1 on resting lymphocytes

Recent studies suggest that some T and B lymphocyte cell lines bind to the integrin lymphocyte function-associated molecule 1 (LFA-1) chiefly through a pathway independent of its two known counter-receptors, intercellular adhesion molecules (ICAMs)-1 and -2. A monoclonal antibody (mAb) was raised that, in combination with blocking mAb to ICAM-1 and ICAM-2, can completely inhibit binding of these cell lines to purified LFA-1. This third ligand, designated ICAM-3 based on its functional relatedness to ICAM-1 and -2, is a highly glycosylated protein of 124,000 Mr. It is well expressed on all leukocytes and absent from endothelial cells. In assays of adhesion of resting lymphocytes to purified LFA-1, ICAM-3 is by far the most functionally important ICAM, implying an important role for ICAM-3 in the generation of immune responses.     

细胞间黏附分子-1与糖尿病尿白蛋白排泄关系的临床研究

目的比较不同程度白蛋白尿糖尿病患者尿液中可溶性细胞间黏附分子-1（sICAM-1）浓度变化并探讨其临床意义。方法收集正常对照组20例，2型糖尿病患者58例，据其24小时尿白蛋白（ALB）每分钟排泄率（UAER）分3组：①正常白蛋白尿（A）组，UAER〈20μg／min，21例；②微量蛋白尿（B）组，20μg/min≤UAER〈200μg／min，20例；③临床蛋白尿（C）组，UAER〉200μg／min，17例。尿sICAM-1检测采用酶联免疫吸附（ELISA）法。结果（1）糖尿病组尿sICAM-1／Ucr比值较对照组显著升高（P〈0．01），并随UAER升高而增加。糖尿病组内，与A组比较，B组水平明显升高（P〈0．05），C组水平进一步升高（P〈0．01）；与B组比较，C组水平也增高（P〈0．05）。（2）相关分析显示：尿sICAM-1／Ucr比值与尿白蛋白呈显著正相关（r=0．852，P〈0．01）。结论2型糖尿病患者尿sICAM-1排泄增加可显示全身或肾脏局部增强的炎症反应并与糖尿病肾病的病情进展有关。     

Intercellular adhesion molecule-1 deficiency prolongs survival and protects against the development of pulmonary inflammation during murine lupus.

One of the characteristic features of the lupus syndrome in humans and mice is the organ-specific accumulation of leukocytes within a variety of different tissues; however, the etiology of this phenomenon remains unclear. The work presented here determined the role of intercellular adhesion molecule (ICAM)-1 in the development of pulmonary leukocyte accumulation by generating MRL/MpJ-Faslpr mice that are genetically deficient in this critical adhesion molecule. Interestingly, these MRL/MpJ-Faslpr ICAM-1 knockout mice exhibit prolonged survival times compared to littermates expressing ICAM-1. We have determined that lack of ICAM-1 completely abrogates the development of pulmonary inflammation but does not prevent the development of autoantibodies, lymphadenopathy, and glomerulonephritis. Furthermore, the lack of pulmonary inflammation was found to be due to decreased migration of leukocytes to the lung rather than decreased in situ proliferation of cells.     

西洛他唑对人脐静脉内皮细胞血管细胞黏附分子1和细胞间黏附分子1mRNA表达的影响

目的观察西洛他唑对人脐静脉内皮细胞（HUVECs）血管细胞黏附分子1（VCAM-1）和细胞间黏附分子1（ICAM-1）mRNA表达的影响,探讨西洛他唑可能的抗动脉粥样硬化作用机制。方法将HUVECs用不同浓度的西洛他唑（0μg/L、0.05μg/L、0.1μg/L、1.0μg/L、10μg/L）溶液处理1小时后,用肿瘤坏死因子α（TNF-α）10μg/L诱导24小时。半定量复合逆转录聚合酶链反应（RT-PCR）测定黏附分子VCAM-1和ICAM-1mRNA的表达。结果 TNF-α能上调VCAM-1和ICAM-1的表达,西洛他唑在一定程度上可抑制上述作用,随着西洛他唑浓度的增加,ICAM-1mRNA表达水平逐步下降,分别为0.239±0.012、0.205±0.012、0.166±0.010、0.136±0.008,VCAM-1mRNA表达水平也逐步下降,分别为0.114±0.048、0.093±0.051、0.083±0.045、0.068±0.039。结论西洛他唑可抑制TNF-α诱导的HUVECs的黏附分子VCAM-1和ICAM-1mRNA表达,提示西洛他唑的抗动脉粥样硬化作用可能是通过阻止血单核细胞向血管内皮细胞聚集和黏附实现的。     

通心络对大鼠脑缺血再灌注模型微血管细胞间黏附分子1和血管细胞黏附分子1表达的影响

背景:现代医学发现通心络制剂除了具有抗凝和抑制血小板聚集作用外,对血管内皮细胞有一定的保护作用。目的:观察中药复方制剂通心络是否影响脑缺血再灌注动物模型黏附分子的表达。设计:随机对照实验。单位:解放军第二军医大学长征医院神经内科。材料:实验于2002-10/2003-01在解放军第二军医大学长征医院神经内科实验室完成。选择雄性SD大鼠25只,随机分为假手术组5只、模型组10只和通心络组10只。方法:线栓法制备大鼠大脑中动脉脑局灶性脑缺血再灌注模型,假手术组除将尼龙线插在颈外动脉接近颈内动脉分叉处外,其余同模型组。通心络组大鼠在缺血再灌注前给予通心络粉剂1.0g/(kg·d),溶在生理盐水中灌胃1周。模型组和假手术组灌胃等剂量生理盐水。各组大鼠麻醉后取脑制备切片,行常规苏木精-伊红染色、免疫组化及原位杂交染色。主要观察指标:①缺血再灌注后细胞间黏附分子1和血管细胞黏附分子1阳性微血管表达数目。②缺血再灌注后细胞间黏附分子1mRNA阳性微血管表达数目。结果:①假手术组手术侧大脑半球皮质和基底节区未见细胞间黏附分子1、血管细胞黏附分子1蛋白和细胞间黏附分子1mRNA阳性微血管表达。②模型组大鼠缺血2h再灌注6h后,缺血侧大脑细胞间黏附分子1、血管细胞黏附分子-1蛋白表达水平和细胞间黏附分子1mRNA表达水平显著升高。③通心络组缺血侧大脑半球皮质和基底节区蛋白和mRNA阳性微血管数较模型组显著降低犤(10.42±1.98),(12.42±2.14)/高倍视野;(8.54±2.00),(11.12±1.56)/高倍视野犦(P<0.05),血管细胞黏附分子1蛋白阳性微血管表达数目无显著变化(P>0.05)。结论:通心络可以降低大鼠脑缺血再灌注后细胞间黏附分子1的转录和翻译过程,有助于减轻脑缺血后的炎症性损伤过程。     

通心络对大鼠脑缺血再灌注模型微血管细胞间黏附分子1和血管细胞黏附分子1表达的影响

背景：现代医学发现通心络制剂除了具有抗凝和抑制血小板聚集作用外，对血管内皮细胞有一定的保护作用。目的：观察中药复方制剂通心络是否影响脑缺血再灌注动物模型黏附分子的表达。设计：随机对照实验。单位：解放军第二军医大学长征医院神经内科。材料：实验于2002—10／2003—01在解放军第二军医大学长征医院神经内科实验室完成。选择雄性SD大鼠25只，随机分为假手术组5只、模型组10只和通心络组10只。方法：线栓法制备大鼠大脑中动脉脑局灶性脑缺血再灌注模型，假手术组除将尼龙线插在颈外动脉接近颈内动脉分叉处外，其余同模型组。通心络组大鼠在缺血再灌注前给予通-15,络粉剂1．0g／（kg-d），溶在生理盐水中灌胃1周。模型组和假手术组灌胃等剂量生理盐水。各组大鼠麻醉后取脑制备切片．行常规苏木精-伊红染色、免疫组化及原位杂交染色。主要观察指标：①缺血再灌注后细胞间黏附分子1和血管细胞黏附分子1阳性微血管表达数目。②缺血再灌注后细胞间黏附分子1mRNA阳性微血管表达数目。结果：①假手术组手术侧大脑半球皮质和基底节区未见细胞间黏附分子1、血管细胞黏附分子1蛋白和细胞间黏附分子1mRNA阳性微血管表达。②模型组大鼠缺血2h再灌注6h后，缺血侧大脑细胞间黏附分子1、血管细胞黏附分子-1蛋白表达水平和细胞间黏附分子1mRNA表达水平显著升高。③通心络组缺血侧大脑半球皮质和基底节区蛋白和mRNA阳性微血管数较模型组显著降低[（10．42&;#177;1．98），（12．42&;#177;2．14）／高倍视野；（8．54&;#177;2．00），（11．12&;#177;1．56）／高倍视野]（P〈0．05），血管细胞黏附分子1蛋白阳性微血管表达数目无显著变化（P〉0．05）。结论：通心络可以降低大鼠脑缺血再灌注后细胞间黏附分子1的转录和翻译过程，有助于减轻脑缺血后的炎症性损伤过程。     

Early up-regulation of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 expression in rats with hemorrhagic shock and resuscitation.

This study evaluated the effect of resuscitation fluids on intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1). Sprague-Dawley rats (n = 36) were subjected to a 27 mL/kg hemorrhage over 5 min followed by a 1 h shock and 1 h resuscitation. Animals groups included: 1) cannulation only (Sham); 2) hemorrhage only (NR); 3) resuscitation with 1:1 shed blood (Blood); 4) resuscitation with 3:1 lactated Ringer's (81 mL/kg, 3LR+); 5) no hemorrhage but infusion with 3:1 lactated Ringer's (3LR); and 6) resuscitation with .36:1 hypertonic saline (7.5%, 9.7 mL/kg, HTS). At the end of resuscitation, the spleen and lung were harvested for detection of adhesion molecule mRNA and protein by RT-PCR and immunostaining. ICAM-1 and VCAM-1 expression exhibited the following pattern: 3LR+ > HTS approximate to 3LR > Blood approximate to NR approximate to Sham. VCAM-1 mRNA in the lung of the 3LR+ group was 2 or more times more than the groups of Sham, NR, Blood, and 3LR (p < .05). ICAM-1 and VCAM-1 mRNA in the spleen was significantly increased in the 3LR+ group compared with the groups of Sham, NR, and Blood (p < .05). Animals in the 3LR+ group showed enhanced staining for ICAM-1 in the pulmonary microvessels and in the marginal and trabecular areas of the spleen. Pulmonary edema and inflammatory cell infiltration were observed only in the 3LR+ group. In summary, resuscitation with LR following hemorrhagic shock induced immediate up-regulation of ICAM-1 and VCAM-1, which was associated with tissue injury. Thus, the type of resuscitation fluid used affected resuscitation injury.     

Intercellular adhesion molecule-1 and CD36 synergize to mediate adherence of Plasmodium falciparum-infected erythrocytes to cultured human microvascular endothelial cells.

We have compared the adhesion of Plasmodium falciparum-infected erythrocytes to human dermal microvascular endothelial cells (HDMEC) and human umbilical vein endothelial cells (HUVEC) and have assessed the relative roles of the receptors CD36 and intercellular adhesion molecule-1 (ICAM-1). HUVEC (a cell line that expresses high levels of ICAM-1 but no CD36) mediate low levels of adhesion, whereas HDMEC (which constitutively express CD36) mediate high levels of adhesion even before ICAM-1 induction ICAM-1 expression leads to yet greater levels of adhesion, which are inhibited both by anti-ICAM-1 and CD36 mAbs, despite no increase in the expression of CD36. The results indicate the presence of a substantial population of infected cells that require the presence of both receptors to establish adhesion. Synergy between these receptors could be demonstrated using a number of parasite lines, but it could not be predicted from the binding of these same parasite lines to purified ICAM-1 and CD36. This phenomenon could not be reproduced using either purified receptors presented on plastic, or formalin-fixed HDMEC, suggesting that receptor mobility is important. This is the first study to demonstrate receptor synergy in malaria cytoadherence to human endothelial cells, a phenomenon necessary for parasite survival and associated with disease severity.     

血清可溶性血管细胞黏附分子-1和可溶性细胞间黏附分子-1与2型糖尿病血管病变的相关性

目的 探讨血清可溶性血管细胞黏附分子-1（sVCAM-1）和可溶性细胞间黏附分子-1（siCAM-1）在2型糖尿病大、小血管病变中的作用。方法 应用酶联免疫吸附试验（ELISA）法检测了62例2型糖尿病患者血浆sVCAM-1和siCAM-1水平,并与20例健康人作对照。结果 糖尿病各组血清sVCAM-1和siCAM-1水平明显高于健康对照组（P〈0．01）,无血管病变组、微血管病变组和大血管病变组的含量逐步升高（P〈0．01）;逐步多元回归分析表明sICAM-1水平与血浆假性血友病因子（vWF）、甘油三酯（TG）、收缩压（SBP）、舒张压（DBP）呈正相关（r=0．43、0．45、0．52、0．62,均P〈0．01）;sVCAM-1水平与TG、胆固醇（TC）及尿白蛋白／肌酐（Alb／Cr）呈正相关（r=0．59、0．46、0．73,均P〈0．01）;多因素logistic回归分析表明sVCAM-1与是否惠有微血管病变显著相关（β=2．48,P〈0．05）,sICAM-1与是否惠有大血管病变显著相关（β=2．46,P〈0．05）。结论 sICAM-1和sVCAM-1参与了2型糖尿病血管病变的发生和发展,可作为早期2型糖尿病患者慢性血管并发症发生的预测及监测指标。     

Influence of single low-density lipoprotein apheresis on the adhesion molecules soluble vascular cellular adhesion molecule-1, soluble intercellular adhesion molecule-1, and P-selectin.

The aim of our study was to investigate the influence of single low-density lipoprotein apheresis (heparin extracorporeal low-density lipoprotein precipitation [HELP]procedure) on plasma concentrations of soluble adhesion molecules (sAMs) such as soluble vascular cellular adhesion molecule-1 (sVCAM-1), soluble intercellular adhesion molecule-1 (sICAM-1), and P-selectin in patients with familial heterozygous hypercholesterolemia and documented coronary artery disease enrolled in a chronic weekly HELP apheresis. Before HELP apheresis, the mean plasma concentration of sVCAM-1 was 515 +/- 119 ng/ml, 204 +/- 58 ng/ml for sICAM-1, and 112 +/- 45 ng/ml for P-selectin. After single HELP apheresis, plasma concentrations of sAM declined significantly by 32 +/- 7%, 18 +/- 15%, and 33 +/- 25% for sVCAM- 1,sICAM-1 and P-selectin, respectively. After a 1 week interval, sAM concentrations rose to approximately the initial values. The concentrations of all sAMs studied were significantly lower in the plasma leaving than entering the filter. Due to filtration, the decline in plasma level of sVCAM-1, sICAM-1, and P-selectin was 62 +/- 19%, 51 +/- 39%, and 67 +/- 22%, respectively. In addition to lipid reduction, single HELP apheresis significantly lowers plasma concentrations of sVCAM-1, sICAM-1, and P-selectin.     

可溶性细胞间黏附分子-1与类风湿关节炎的相关性研究

目的进一步探讨可溶性细胞间黏附分子-1（sICAM-1）在类风湿关节炎（RA）中的作用。方法采用放射免疫测定法对34例RA患者及30例健康体检者血清、关节液中sICAM-1进行检测。结果所测静脉血清sICAM-1浓度,RA组显著高于健康对照组,差异有统计学意义（P〈0．001）;RA未治疗组显著高于治疗后未复发组,差异有统计学意义（P〈0．001）,但与治疗后复发组比较,差异无统计学意义（P〉0．05）;RA患者关节液中sICAM-1明显高于血清中的水平,二者差异有统计学意义（P〈0．05）,而未治疗组与治疗后复发组关节液中sICAM-1水平差异无统计学意义（P〉0．05）。结论sICAM-1在RA发病中起着重要作用,可作为判断病情严重性的指标用于监测RA的活动及疗效。     

Monocyte attachment to activated human vascular endothelium in vitro is mediated by leukocyte adhesion molecule-1 (L-selectin) under nonstatic conditions

The receptors that mediate monocyte adhesion to cytokine-stimulated endothelial monolayers were assessed using a nonstatic (rotating) cell-attachment assay. In this system, leukocyte adhesion molecule-1 (LAM-1) (L-selectin) mediated a major portion (87 +/- 15% at 37 degrees C) of monocyte attachment to activated endothelium. mAb blocking of endothelial leukocyte adhesion molecule-1 (41% inhibition), CD18 (36%), and vascular cell adhesion molecule-1 (25%) function had lesser effects on attachment. These results suggest that LAM-1 may serve an important role in monocyte attachment to endothelium at sites of inflammation.     

细胞间黏附分子-1在高血压左室肥厚发病中的作用及丹参酮ⅡA对其表达的影响

目的:探讨细胞间黏附分子-1(ICAM-1)在高血压左室肥厚发生中的作用及丹参酮ⅡA对其表达的影响.方法:12周龄雄性Wistar-Kyoto(WKY)大鼠和自发性高血压大鼠(SHR)共30只,随机分为对照组、高血压组、丹参酮ⅡA组.丹参酮ⅡA组经尾静脉连续注射丹参酮ⅡA 治疗12周.断头处死大鼠后留取心肌标本,进行苏木素-伊红(HE)、范吉逊(VG)染色,观察心肌细胞形态和胶原分布情况;免疫组化染色及ED1标记显示心肌巨噬细胞浸润;逆转录-聚合酶链反应检测心肌ICAM-1 mRNA表达;酶联免疫吸附试验(ELISA)检测ICAM-1的蛋白表达.结果:与对照组WKY大鼠比较,SHR组肥厚心肌中ICAM-1的mRNA及蛋白表达均显著增加(P<0.01和P<0.05),巨噬细胞浸润明显(P<0.01).应用丹参酮ⅡA治疗后,SHR组的心肌ICAM-1的mRNA及蛋白表达水平均显著下调(P<0.01和P<0.05),巨噬细胞浸润数减少(P<0.05),心肌细胞肥大和间质纤维化程度明显减轻.结论:心肌ICAM-1过度表达及其介导的炎性细胞浸润在高血压左室肥厚的发病过程中具有重要作用;丹参酮ⅡA抑制左室肥厚的效应可能与其下调ICAM-1表达,减少炎性细胞的心肌浸润有关.     

Increased binding of synovial T lymphocytes from rheumatoid arthritis to endothelial-leukocyte adhesion molecule-1 (ELAM-1) and vascular cell adhesion molecule-1 (VCAM-1).

The infiltration of the synovial membrane (SM) by mononuclear cells, mostly T cells, is a typical histopathological feature associated with rheumatoid arthritis (RA). The entry of T lymphocytes into the SM is believed to be mediated by a number of molecules in the endothelium that are induced in response to a series of inflammatory mediators. In this study, we have investigated the adhesion of synovial T cells from RA patients to two endothelial ligands: endothelial-leukocyte adhesion molecule-1 (ELAM-1), the only selectin known to function as a vascular addressin for T cells, and vascular cell adhesion molecule-1 (VCAM-1), the cellular ligand of VLA-4. Our results clearly demonstrate that synovial T cells isolated from both SM and synovial fluid (SF), bearing an activated and memory phenotype, displayed an enhanced capacity to interact with these two endothelial molecules as compared with T cells from peripheral blood (PB) either of the same RA patients or healthy donors. A further enhancement of VLA-4-mediated T cell binding to VCAM-1 and fibronectin could be observed when already in vivo-activated synovial T cells were stimulated in vitro with phorbol esters, suggesting the existence of several cellular affinity levels for both very late activation-4 (VLA-4) ligands. Moreover, both PB and synovial T cells from RA patients exhibited strong proliferative responses when they were cultured with either fibronectin or VCAM-1 in combination with submitogenic doses of anti-CD3 mAb. This increased endothelial binding ability of synovial T lymphocytes together with their proliferation in response to the interaction with VCAM-1 and fibronectin may represent important mechanisms in the regulation of T cell penetration and persistence in the chronically inflamed SM of RA.     

大鼠脑缺血再灌注区细胞间粘附分子1表达与白细胞浸润的实验研究

目的：观察大鼠脑缺血－再灌注后不同时间缺血区细胞间粘附分子－１（ＩＣＡＭ－１）的表达和中性粒细胞的浸润以及神经细胞的损伤情况。方法：４０只Ｗｉｓｔａｒ大鼠分为对照组、假手术组和缺血２小时再灌注２、４、１２、２４、４８、９６小时组,分别用免疫组织化学和组织切片方法检测大脑中动脉阻塞２小时再灌注不同时间点局部脑组织ＩＣＡＭ－１蛋白表达及中性粒细胞浸润情况。结果：大鼠脑缺血 灌液２小时局部脑组织ＩＣＡＭ     

2型糖尿病患者血清sICAM-1和sVCAM-1的检测与大血管病变的关系

目的　探讨 2型糖尿病患者血清可溶性细胞间黏附分子 1(solubleintercellaradhesionmolecule 1,sICAM 1)和可溶性血管细胞黏附分子 1(solublevascularcelladhesionmolecule 1,sVCAM 1)与大血管病变的关系。方法　测定 76例 2型糖尿病患者及 4 8例健康对照者血清sICAM 1和sVCAM 1水平 ,76例 2型糖尿病患者分为大血管病变组 (2 8例 )与无大血管病变组 (48例 ) ,比较三组间sICAM 1和sVCAM 1的水平。并对糖尿病组中颈总动脉内膜厚度 (intima mediathickness,IMT)与sICAM 1和sVCAM 1作单因素相关分析。结果　 2型糖尿病患者中无大血管病变组及有大血管病变组的血清sICAM 1和sVCAM 1水平分别高于健康对照者 (P <0 .0 5 ,P <0 .0 1) ,有大血管病变者又高于无大血管病变者 (P <0 .0 5 )。糖尿病组中颈总动脉IMT分别与sICAM 1和sVCAM 1呈正相关 (r =0 .2 0 2 ,P <0 .0 5 ;r =0 .35 8,P <0 .0 1)。结论　 2型糖尿病患者血清sICAM 1和sVCAM 1水平的升高 ,表明了体内存在血管内皮细胞功能紊乱和白细胞的激活 ,并参与了大血管病变的发生发展过程 ,可作为病情监测的血清学指标