白细胞黏附分子CD54、CD62L、CD44在慢性肺源性心脏病患者外周血白细胞的表达

目的探讨白细胞黏附分子CD54、CD62L、CD44在慢性肺源性心脏病（chronic cor pulmonale,CCP）外周血白细胞（PBC）上的表达。方法采用流式细胞术,选用单克隆抗体检测CCP患者40例（B组：B1组急性加重期20例,B2组经治疗后进入缓解期20例）外周血中性粒细胞（N）、淋巴细胞（L）、单核细胞（M）表面CD54、CD62L及CD44的表达,同时设立慢性阻塞性肺疾病（chronic obstructive pulmonary disease,COPD）患者40例（A组）及健康者20例（C组）作为对照组。结果B1组、B2组N和LCD54,MCD54和CD62L阳性表达率较C组显著升高（P〈0.05）,但B1组与B2组间无显著性差异（P〉0.05）;B1组、B2组N和LCD62L,及N、L和MCD44阳性表达率与C组间均无显著性差异（P〉0.05）。A组LCD54、CD62L和CD44,MCD54阳性表达率较C组显著升高（P〈0.05）;A组NCD62L阳性表达率较C组降低（P〈0.05）;A组NCD54、MCD62L、N和MCD44阳性表达率与C组间均无显著性差异（P〉0.05）。B组N和LCD54,MCD54和CD62L阳性表达率较C组显著升高（P〈0.01）;B组N和LCD62L,N、L和MCD44阳性表达率与C组间均无显著性差异（P〉0.05）。B组NCD54、MCD62L阳性表达率较A组显著升高（P〈0.05）;A组LCD44阳性表达率较B组显著升高（P〈0.05）;A组L和MCD54、N和LCD62L、N和LCD44阳性表达率与B组间均无显著性差异（P〉0.05）。结论CCP患者通过外周血N表面CD54、L表面CD54、M表面CD54和CD62L表达上调,参与自身的病理生理过程。在从COPD发展成为CCP的过程中,L和M表面CD54,尤其是N表面CD54和M表面CD62L表达上调可能在慢性肺动脉高压的形成中起重要作用。而白细胞黏附分子CD44可能不起重要作用。     

CD44s和CD44v6在肺癌组织中的表达及意义

采用免疫组化法检测107例肺癌组织中标准型CD44（CD44s）和变异型CD44（CD44v）6的表达,结果，17例小细胞肺癌（SCLC）中，CD44v6和CD44s均无表达;非小细胞肺癌（NSCLC）中，CD44v6和CD44s在鳞癌中的阳性表达率（81．0％和83．3％）均高于腺癌（39．6％和54．2％），P均〈0．05;无淋巴结转移的NSCLC中，CD44v6阳性表达率（34．0％）低于CD44s（78．0％）。P〈0．05；有淋巴结转移的NSCLC中．CD44v6阳性表达率（90．0％）高于CD44s（55．0％），P〈0．05。NSCLC的CD44v6和CD44s表达与其病理类型、临床分期、肿瘤分级及淋巴结转移均有关（P均〈0．05）。认为CD44v6和CD44s可以作为鉴别SCLC与NSCLC及判断肺癌病理类型、临床分期、肿瘤分级及淋巴结转移的参考指标。     

非小细胞肺癌外周血CD44和CD54表达的定量研究

目的 探讨非小细胞肺癌患者外周血淋巴细胞中CD44和CD54表达与临床病理的关系。方法 应用流式细胞术对50例肺癌患者外周血淋巴细胞中CD44和CD54表达与临床病理的关系。方法 应用流式细胞术对50例肺癌患者外周血淋巴细胞中CD44和CD54表达进行荧光免疫检测,并与正常对照组（30名）及肺部良性病变组（25例）进行对比研究。结果 50例肺癌患者外周血淋巴细胞中CD44和CD54表达明显高于正常对照组及良性病变组（P＜0．01）。良性病变组和正常对照组之间CD44和CD54的表达比较,差异无显著性（P＞0．05）。肺癌伴淋巴结转移CD44和CD54高于不伴淋巴结转移者（P＜0．01）;Ⅲ期、Ⅳ期和Ⅰ期、Ⅱ期之间CD44表达比较,差异有显著性（P＜0．01）;Ⅳ期和Ⅰ期、Ⅱ期、Ⅲ期之间CD54表达比较,差异有显著性（P＜0．01）。CD44和CD54表达与肺癌组织学分级有明显相关性（P＜0．05或0．01）;与鳞癌和腺癌没有相关性。结论 应用流式细胞仪检测CD44和CD54的表达水平可作为肺癌转移和预后的指标。     

妊娠早期孕妇CD56^brightCD16^-uNK、pNK细胞中CD44的表达变化及意义

目的观察妊娠早期妇女CD56^brightCD16^-子宫NK细胞（uNK细胞）和CD56^brightCD16^-外周血NK细胞（pNK细胞）表面cD。的表达变化,探讨CD56^brightCD16^-uNK细胞中CD44表达与母胎界面免疫耐受形成的关系。方法采集20例孕5—9周的正常妊娠妇女蜕膜和外周血以及20例正常非孕健康妇女外周血,用流式细胞仪检测其中CD56^brightCD16^-NK细胞的数量及其表面CD44的表达。结果早期妊娠妇女子宫蜕膜淋巴细胞中CD56^brightCD16^-NK细胞占71．86％±6．22％,CD56^brightCD16^-uNK细胞中CD44的阳性表达率为34．65％±9．96％,显著低于CD56^brightCD16^-pNK细胞的99．55％±0．35％,P〈0．05。非孕期妇女CD56^brightCD16^-pNK细胞CD44阳性表达率为99．66％±0．29％,与妊娠早期孕妇相近,但孕早期妇女外周血CD56^brightCD16^-NK细胞CD44平均荧光强度（MFI）为241．71±62．41,正常未孕妇女为354．62±41．28,两者相比P〈0．05。结论妊娠早期子宫蜕膜的淋巴细胞主要为CD56^brightCD16^-uNK细胞。CD56^brightCD16^-uNK细胞中CD44的表达明显低于pNK。这可能是妊娠早期维持母胎界面免疫耐受的重要因素。     

CD44s mRNA在胃癌组织中的表达及其临床意义

目的探讨CD44s mRNA在胃癌组织中的表达及其临床意义。方法采用核酸原位杂交技术检测66例胃癌（胃癌组）、25例浅表性胃炎（胃炎组）和25例胃上皮不典型增生（增生组）中CD44s mRNA的水平。结果胃炎组无阳性表达;增生组中阳性率为20％;在胃癌组中阳性率为62．12％,胃癌组低分化组织中阳性率明显高于高分化组织（P〈0．05）,有淋巴结转移组阳性率明显高于无淋巴结转移组（P〈0．05）。结论CD44s mRNA表达与胃癌组织分化程度和转移有相关性;CD44s mRNA基因水平可作为判断胃癌病情和预后的指标。     

子宫内膜腺癌组织中CD147、MMP-2的表达变化及意义

目的观察子宫内膜腺癌组织中CD147、基质金属蛋白酶2（MMP2）的表达变化，并探讨其临床意义。方法采用免疫组化SP法检测53例子宫内膜腺癌（A组）、35例子宫内膜增殖症（B组）及19例增生期子宫内膜（C组）组织中的CD147、MMP-2蛋白。结果A组CD147、MMP2蛋白阳性表达44、49例，B组分别为16、20例，C组分别为7、9例；各组间比较，P均〈0．05。CD147蛋白表达与子宫内膜癌组织分级有关（P〈0．05）。子宫内膜腺癌组织中CD147和MMP2蛋白表达呈正相关（r=0．441，P〈0．01）。结论子宫内膜腺癌组织中CD147、MMP2的表达增高，二者在子宫内膜腺癌的发展恶化、侵袭和转移中发挥重要作用。     

CD44在糖尿病肾病中的表达及意义

根据尿白蛋白排泄率（UAER），将60例2型糖尿病（T2DM）患者分为三组，即正常白蛋白尿组（A组）、微量白蛋白尿组（B组）、临床白蛋白尿组（C组）。应用流式细胞免疫学方法测定三组患者和健康对照者（对照组）外周血中CD44阳性细胞数，并将CD44表达与其空腹血糖，糖化血红蛋白、胆固醇、甘油三酯、高密度脂蛋白、UAER、尿N-乙酰-β-D-氨基葡萄糖苷酶（NAG）水平进行相关性分析。结果显示，T2DM患者的外周血CD44阳性细胞率均显著高于对照组（P〈0．01），B、C组高于A组（P〈0．01）。T2DM患者尿NAG均高于对照组．但A、B、C组间无统计学差异（P〉0．05）。CD44表达与尿NAG呈正相关（P〈0．01），与其他指标无相关性。提示外周血CD44可作为监测糖尿病肾病（DN）病情变化的指标之一，NAG与CD44在DN病变过程中可能有协同性。     

妊娠期甲型H1N1流感患者T淋巴细胞亚群变化

目的分析妊娠期重症甲型H1N1流感患者T淋巴细胞亚群变化,探讨患者的免疫病理机制及T淋巴细胞亚群检测在妊娠期合并重症甲型H1N1流感诊断中的临床意义。方法选择沧州地区2009年11月10日－12月31日确诊重症／危重症甲型H1N1流感56例。选取其中妊娠期患者32例（A组）,并设置正常妊娠组（B组）及对照组。取外周血检测T淋巴细胞亚群和NK细胞。结果白细胞总数A组低于B组（P〈0．05）,B组高于对照组（P〈0．05）;淋巴细胞绝对值及百分比A组低于B组及对照组（P〈0．05）。A组外周血总T细胞、CD4^＋T细胞、CD8^＋T细胞、CD15＋56NK细胞绝对值及CD4／CD8比值均低于B组、对照组（P〈0．05）;B组较对照组上述指标均降低（P〈0．05）。结论妊娠期免疫耐受所致细胞免疫功能抑制可能参与重症H1N1流感的疾病发生发展过程,应用细胞免疫增强剂可能对疾病过程有积极影响。     

HBsAg阳性患者HBcAg表达与肝组织淋巴细胞数量变化的关系

目的研究HBsAg阳性患者HBcAg表达与肝组织中T、B淋巴细胞、NK细胞、Kupffer细胞数量等临床指标变化的关系。方法选取50例HBsAg阳性表达的患者肝组织及23例肝血管瘤患者瘤旁正常肝组织,分别进行CD3、CD57、CD20、CD68及HBcAg免疫组织化学染色;用病理图像分析仪测量每例患者肝组织和正常肝组织每平方微米面积阳性细胞数。结果HBsAg阳性表达的患者肝组织中T淋巴细胞、B淋巴细胞、NK细胞和Kupffer细胞数量明显多于正常肝组织,以T淋巴细胞数量增加最为显著（P〈0．05）,HBcAg阳性表达组与HBcAg阴性表达组肝组织中T淋巴细胞、B淋巴细胞、NK细胞和Kupffer细胞数量变化无统计学意义（P〉0．05）。HBcAg阳性表达组比HBcAg阴性表达组外周血的AFP、ALT含量高（P均〈0．05）,AST、GGT、ALP、白蛋白减少（P均〈0．05）,A／G比例降低（P〈0．01）。结论各免疫细胞数量变化与膜型HBsAg的表达有关,与核型HBcAg表达无关;但核型HBcAg的表达与各临床指标的改变密切相关。     

不同来源的CD34^＋细胞归巢相关分子的表达

目的 研究不同来源CD34^＋细胞归巢相关分子（HRM）的表达情况。方法采用免疫磁珠法（MACS）分选不同来源的CD34^＋细胞，免疫荧光标记流式细胞仪测定HRM的表达。结果骨髓（BM）、动员后的外周血（mPB）及脐血（UCB）来源的CD34^＋细胞均高表达细胞黏附分子CD49d、CD49e、CD54、CD11a、CD62L、CD44、CD31。UCB来源的CD34^＋细胞表面表达的细胞黏附分子中，CD49e表达显著低于BM和mPB来源的CD34^＋细胞（P〈0．05），CD54表达显著低于mPB来源者（P〈0．05），CXCR4表达显著低于BM来源者（P〈0．05）。结论UCB来源的造血干／祖细胞归巢能力低可能是UCB移植造血重建延迟的原因之一。     

白细胞粘附分子在慢性阻塞性肺疾病及肺心病发病中作用的探讨

目的：探讨白细胞粘附分子在慢性阻塞性肺疾病（COPD），慢性肺原性心脏病（肺心病）发病机制中的作用，及抗白细胞粘附疗法在肺心病治疗中的疗效。方法：采用流式细胞术，用单克隆抗一量测定42例COPD患（稳定期），41例肺心病患（稳定期）周围血中白细胞粘附分子CD11a,CD11b,CD18,CD54的阳性表达率，并以24名健康人作正常对照，41例肺心病患分为2组，治疗组20例，服用火把花根片（1次3片，1日3次），对照组21例，测定20例服火把花根片后的肺心病患周围血中白细胞粘附分子CD11a,CD11b,CSD18,CD54，淋巴细胞表面CD11a的阳性表达率明显高于正常对照组（P＜0．05），肺心病患组血液中性粒细胞表达CD11a,CD11b,CD18,CD54，单核细胞表面CD11a,CD18,CD54，淋巴细胞表面CD18较正常对照组明显增强（P＜0．05）；服火把花根片后，肺心病治疗组中性粒细胞表达CD11a,CD11b,CD18,CD54，单核细胞表面CD11a,CD18,CD54,淋巴细胞表达CD18较服药前肺心病组有显下降（P＜0．05），余各型均无显差异。结论：COPD患通过单核细胞粘附分子CD11a/CD18,CD11b/CD18,CD54的表达上调，肺心病患通过中性粒细胞表面粘附分子CD11a/CD18,CD11b/CD18,CD54及单核细胞表达CD11/CD18,CD54的表达上调，使白细胞与内皮细胞粘附明显增强，参与各自疾病的病理发展过程，火把花根通过肺心病中性粒细胞表面粘附分子CD11a/CD18,CD11b/CD18,CD54及单核细胞表达CD11a/CD18,CD54的表达下调，使白细胞与内皮细胞的粘附下降，阻止肺心病的发展。     

Activation of leukocytes by postprandial lipemia in healthy volunteers

Activation of leukocytes is obligatory for inflammation and atherogenesis by adhering to the endothelium via specific ligands. Although in vitro studies have shown that triglycerides (TG) can activate leukocytes, it is unknown whether this occurs in vivo. Using flowcytometry, we studied the expression of leukocyte activation markers CD11A, CD11B, CD62L (all involved in endothelium adhesion) and CD66B (a neutrophil degranulation marker) during a 6 h fat challenge (50 g/m2) and a water test in 10 healthy males (52 +/- 3 years). After fat, neutrophil counts were increased between t=1 and t =6 h, with a maximum at t=3 h (+32% versus t=0, P <0.05), while they remained unchanged after water. Both tests showed gradual lymphocyte count increments. The expression of activation markers on lymphocytes was low and showed comparable responses after both tests. After fat, a significant increase up to a maximum at t=6 h was seen for CD11B on monocytes and on neutrophils for CD11B, CD62L and CD66B. Postprandial activation of monocytes and neutrophils was higher after fat than after water. The maximal postprandial TG increment was significantly related to the increase of CD11B on monocytes (Pearson's R=0.64, P <0.05). In conclusion, postprandially there is a TG-specific increase of neutrophil counts and increased activation of monocytes and neutrophils. These results are suggestive of a pro-inflammatory situation that may correspond with increased adhesive capacity of these cells contributing to the inflammatory component of atherosclerosis.     

Peripheral blood mononuclear cell CD62L and CD11a expression and soluble interstitial cell adhesion molecule-1 levels following infused isoproterenol in hypertension

OBJECTIVES : Increasingly, studies indicate that alterations in leukocyte and endothelial cell adhesion molecules may enhance atherosclerotic processes in human hypertension. beta-adrenergic receptor activation has long been implicated in the aetiology and/or maintenance of hypertension and also has significant effects on leukocyte and endothelial adhesion molecules. This study therefore examined the effects of hypertension on peripheral blood mononuclear cell CD62L and CD11a expression and circulating soluble interstitial cell adhesion molecule (ICAM)-1 (sCD54) levels following infusion of the non-specific beta-adrenergic agonist isoproterenol. DESIGN : In the setting of a General Clinical Research Center, 15 hypertensive and 20 normotensive subjects underwent an infusion of isoproterenol consisting of two sequential 15 min fixed-order doses of 20 and 40 ng/kg per min. Flow cytometry was used to quantify lymphocyte and monocyte populations and adhesion molecules, and ELISA was used to quantify sCD54 levels. RESULTS : As expected, isoproterenol led to a significant increase in the number of circulating lymphocytes (P < 0.001) and monocytes (P < 0.01). The number of circulating CD3+CD8+CD62Llow T cytotoxic cells increased following isoproterenol (P < 0.001) and this increase was greater in hypertensives than in normotensives (P < 0.05). Isoproterenol led to a decrease in surface density of CD62L (P < 0.001) and an increase in surface density of CD11a (P < 0.001) in all subjects. Hypertensives had a significantly lower CD62L density (P = 0.01) and higher CD11a density on lymphocytes (P = 0.002) compared to normotensives. sCD54 levels were unchanged following isoproterenol but were elevated in hypertensives (P < 0.05). CONCLUSIONS : A beta-adrenergic-induced environment of increased CD62Llow/CD11ahigh leukocytes, coupled with existing endothelial CD54 activation, could support basic atherosclerotic processes of increased peripheral blood mononuclear cell-endothelial adhesion in hypertension.     

Deficient expression of adhesion molecules by human CD5- B lymphocytes both after bone marrow transplantation and during normal ontogeny

Despite the relatively early reconstitution of blood B-lymphocyte counts observed in patients treated with bone marrow transplantation (BMT), these patients undergo a prolonged phase of humoral immunodeficiency. Adhesion molecules perform relevant functions in many cell types. The present study examines the expression of several adhesion molecules on human B lymphocytes newly formed after BMT. Blood B cells from 38 patients were studied by flow cytometry and three-color analysis. Blood CD5- B lymphocytes obtained at an early stage after BMT (2 to 4 months) showed a markedly low expression of the adhesion molecules CD54, CD44, CD11a, and CD62L. However, these cells exhibited a normal expression of other molecules including CD29, CD19, CD20, and DR. This deficiency was progressively corrected, reaching normal levels in the late post-BMT period (12 to 15 months). In contrast, CD54, CD44, CD11a, and CD62L expression on the patients' CD5+ B lymphocytes was found to be consistently normal. Deficient adhesion molecule expression on CD5- B cells in the early post-BMT period was similarly observed in patients treated with either an allo-BMT (n = 24) or an auto-BMT (n = 14). Because the post-BMT period mimics normal ontogeny, adhesion molecule expression was also investigated in cord-blood B lymphocytes. Cord-blood CD5- B lymphocytes, in contrast to CD5+, also expressed CD54, CD44, CD11a, and CD62L at levels much lower than those found in normal adults. Present data suggest that progressive expression of CD54, CD44, CD11a, and CD62L seems to be a part of the maturational program of CD5- B lymphocytes during both post-BMT and normal development periods. This observation may help to explain the humoral immunodeficiency observed in both conditions.     

单核细胞和血小板CD40L高表达及血小板CD62P高含量与急性冠脉综合征的关系

目的探讨急性冠脉综合征(ACS)外周血单核细胞和血小板表达CD40L及血小板CD62P含量的变化及意义。方法应用间接免疫荧光流式细胞仪测定患者与对照组血单核细胞和血小板表达CD40L水平及血小板CD62P含量。结果发现急性冠脉综合征患者(ACS)单核细胞和血小板表达CD40水平及血小板CD62P含量均显著高于正常对照者(NS)(P<0.01)和稳定型冠心病患者(SA)(P<0.05或P<0.01)。结论急性冠脉综合征患者外周血单核细胞和血小板表达CD40L及血小板CD62P含量可能与ACS的发生有关,是动脉粥样硬化斑块不稳定的标志。     

Neutrophil surface expression of CD11b and CD62L in diabetic microangiopathy

The aims of the study are (1) assessment of cell surface expression of adhesion molecules CD11b and CD62L on peripheral blood neutrophils in patients with type 2 diabetes and microangiopathy; (2) analysis of serum levels of soluble adhesion molecules: E-selectin (sE-selectin), soluble intercellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1) and von Willebrand factor (vWF) and; (3) evaluation of systemic inflammatory markers like interleukin-6 (IL-6), soluble interleukin-6 receptor (IL-6Rs), high sensitivity C-reactive protein (hsCRP) and fibrinogen. Thirty patients with type 2 diabetes and microangiopathy were enrolled in the study. The study group was compared to 22 patients with type 2 diabetes without microangiopathic compliations. The control group included 20 healthy volunteers. Flow cytometry was used to analyse surface expression of adhesion molecules. Both inflammatory markers and soluble adhesion molecules were determined by immunoenzymatic assay. A significant increase in neutrophil surface CD11b expression (P < 0.01) as well as decrease in surface CD62L expression (P < 0.01) were observed in the group with diabetic microangiopathy in comparison with diabetic group without microangiopathic complications and healthy controls. Moreover, significantly higher concentrations of sICAM-1 (P < 0.05), sVCAM-1 (P < 0.05), sE-selectin (P < 0.05), vWF (P < 0.01), hsCRP (P < 0.01), IL-6 (P < 0.01) and fibrinogen (P < 0.001) were also found in patients with microangiopathy in comparison with the control group. IL-6Rs concentrations did not significantly vary between groups. We concluded (1) diabetic microangiopathy is accompanied by increase in CD11b expression and decrease in CD62L expression on peripheral blood neutrophils; (2) in diabetic microangiopathy rise in CD11b expression indicates neutrophil activation and intensified adhesion; (3) the development of diabetic microangiopathy is accompanied by an increase in soluble adhesion molecules and inflammatory markers concentrations in the blood.     

A marked decrease in l‐selectin expression by leucocytes in infants with Bordetella pertussis infection: leucocytosis explained?

OBJECTIVE: Infants with Bordetella pertussis infection (whooping cough) have an unexplained lymphocytosis and leucocytosis characterized by an increase in small lymphocytes with convoluted and cleaved nuclei. To characterize these cells immunophenotyping using multiparameter flow cytometry was performed on leucocytes from a group of 11 infants aged 3-6 months with proven pertussis and from uninfected control subjects. METHODOLOGY: The panel of monoclonal antibodies used to elucidate leucocyte subtypes included activation, adhesion, costimulatory, memory, T-helper (Th) 1 and Th2 markers. RESULTS: Patients with pertussis showed an increase in absolute numbers of neutrophils, monocytes, T lymphocytes (both CD4 and CD8), B lymphocytes (including CD10+/CD19+ haematogones) and natural killer (NK) cells. All leucocyte subgroups showed a marked decrease in L-selectin (CD62L) expression. The expression of other adhesion molecules CD11a, CD44 and CD54 on all leucocyte subgroups was unchanged. Expression of costimulatory molecules, CD49D and CD28 on T cells and CD80 and CD86 on monocytes, was unchanged. Lymphocyte activation markers CD69, CD25 and HLA-DR were unchanged. There was an increase in CD45RA+/CD45RO+/CD4+ cells (activated) and CD62L-/CD45RO+/CD4+ cells (Th1-like) but no increase in CD7-/CD4+ T cells (Th2-like). CONCLUSIONS: L-Selectin expression mediates extravasation of leucocytes into tissues and is important for homing of peripheral blood lymphocytes to lymph nodes. The significant down-regulation of L-selectin on leucocytes in pertussis infection may prevent leucocyte migration to areas of infection and homing and adhesion of T and B cells to peripheral lymphoid tissues. The increase in lymphocytes with Th1 phenotype may be required for effective immune response to the infective organism. These data provide a possible explanation for the absolute leucocytosis observed in this disease.     

Activated peripheral blood and endothelial cells in thalassemia patients

BACKGROUND AND OBJECTIVES: Thalassemia patients have alterations in the expression of some activation and adhesion molecules on peripheral blood lymphocytes. We studied cell surface antigens on peripheral blood cells associated with the activation of these cells and soluble molecules produced by activated endothelium. DESIGN AND METHODS: We investigated the expression of CD11b, CD18, CD35, CD43, CD44, and CD69 on the peripheral blood monocytes, Cd11b, CD18, CD35, CD43, CD44, CD67 on peripheral blood neutrophils and CD38 and CD69 on peripheral blood lymphocytes. We studied 68 transfusion-dependent thalassemics (group A), 10 transfusion non-dependent thalassemics (group B), 18 beta-thalassemia carriers (group C), and 28 normal individuals. Relative fluorescence intensity was used to determine the antigen density. Analysis was performed with an EPICS ELITE flow cytometer. Furthermore, soluble intercelullar adhesion molecule 1 (sICAM-1), soluble vascular adhesion molecule 1 (sVCAM-1), and E-selectin, tumor necrosis factor (TNF) alpha, and interleukin (IL) 1beta were measured in the plasma of patients by enzyme-linked immunometric assay. Results: The expression of CD11b, CD18, and CD69 on the monocytes of group A was significantly greater than in groups B and C and in controls, while CD44 was significantly downregulated in group A. CD11b, CD18, CD35, CD44, and CD67 on the surface of neutrophils and CD38 and CD69 on the surface of lymphocytes were also overexpressed in group A. CD44 was downregulated on the monocytes and upregulated on the neutrophils of the patients compared to controls. The levels of sICAM-1, sVCAM-1, E-selectin, TNF-alpha, and IL-1beta in the serum of patients in groups A and B were higher than those in group C and the controls. CONCLUSION: Endothelial activation markers are significantly increased in thalassemia patients, and activated blood cells circulate in the peripheral blood. These may be related to the vascular complications in these patients and might be useful markers for the follow-up of the vascular disease.     

冠心病患者中性粒细胞和单核细胞CD11b/CD18表达的研究

目的 :探讨不同类型冠心病患者中性粒细胞和单核细胞膜 CD11b/CD18表达的变化。方法 :选择经冠状动脉造影确诊的 49例心绞痛患者 ,30例急性心肌梗死患者和 2 0例正常人 ,用流式细胞仪直接免疫荧光法检测中性粒细胞和单核细胞膜 CD11b/CD18表达。结果 :冠心病患者中性粒细胞和单核细胞膜 CD11b/CD18表达较正常对照组均显著增加 （P<0 .0 1） ;不稳定性心绞痛和急性心肌梗死患者中性粒细胞和单核细胞膜 CD11b/CD18表达显著高于稳定性心绞痛患者 （P<0 .0 1）。与正常对照组比较 ,心绞痛患者组中性粒细胞和单核细胞计数无变化 （P>0 .0 5 ） ,而急性心肌梗死组明显增加 （P<0 .0 1）。急性心肌梗死患者中性粒细胞和单核细胞膜 CD11b/CD18表达与梗死范围无关。结论 :冠心病患者中性粒细胞和单核细胞膜 CD11b/CD18表达明显增加 ,其增加程度与心肌缺血的类型有关。