黏附分子CD56、CD44、CD54、CD11a在急性髓系白血病骨髓中的表达及意义

目的:探讨黏附分子CD56、CD44、CD54、CD11a在急性髓系白血病(AML)骨髓中的表达情况及临床意义。方法:流式细胞仪检测57例AML患者和20例正常对照者骨髓单个核细胞表面CD56、CD44、CD54、CD11a的表达水平,分析其与AML患者白细胞计数、白细胞淤滞及早期病死率的关系。结果:1CD56仅在AML组表达(AML组表达率为35.1%,正常对照组0,P0.05),其在AML高白细胞(HAML)组的表达率(53.3%)高于AML非高白细胞(NHAML)组(28.6%),白细胞淤滞组(62.5%)高于无白细胞淤滞组(28.9%)(P0.05);2AML患者骨髓单个核细胞表面CD44的平均荧光强度在HAML组显著高于NHAML组(P0.05),其表达与AML患者外周血白细胞计数呈正相关(r=0.446,P0.01)。CD56、CD54、CD11a在HAML组与NHAML组、无白细胞淤滞组与白细胞淤滞组的平均荧光强度均差异无统计学意义(P0.05)。3AML患者中HAML组、白细胞淤滞组患者的早期病死率(33.3%、25.0%)分别明显高于NHAML组、无白细胞淤滞组(0、0)。结论:CD56在HAML患者和白细胞淤滞患者有更高的表达率,有可能是AML患者预后不良的因素之一;CD44在AML患者骨髓中的表达水平与外周血白细胞计数呈正相关,可能参与HAML的发生。CD54、CD11a与HAML及白细胞淤滞的关系不十分密切。     

急性髓系白血病骨髓单个核细胞CD11a的表达及临床意义

目的:探讨淋巴细胞功能相关抗原-1(LFA-1)的α链CD11a在急性髓系白血病(AML)的表达情况及临床意义。方法:采用免疫酶标ABC法检测25例初治AML患者和8例血液系统非恶性肿瘤患者为对照的骨髓单个核细胞CD11a的表达,并追踪观察AML患者的疗效。结果:CD11a在AML患者骨髓单个核细胞的表达率(37.02±13.30)%,明显低于对照组(87.13±5.38)%(P<0.05)。化疗后未缓解组AML患者发病时骨髓单个核细胞CD11a的表达率(47.09±10.55)较完全缓解组(29.11±9.36)%高(P<0.05)。结论:CD11a在AML患者骨髓单个核细胞表达异常,可能与白血病细胞逃脱机体免疫监控及从造血微环境释出有关。检测AML患者骨髓单个核细胞CD11a的表达水平对AML的预后判断有一定意义。     

动脉样硬化患者CD11a、CD11b和CD18表达的初步研究

目的：探讨动脉粥样硬化和白细胞功能相关抗原（LFA－1即CD11a/CD18）以及巨噬细胞分化抗原（Mac-1即CD11b/CD18)等细胞粘附分子表达的关系。方法：用碱磷酶抗磷磷酶（A－PAAP）桥联酶免疫细胞化学染色法检测冠心病患者外周血单个核细胞表面的CD11a、CD11b和CD18。结果心病患者CD11a、CD11b、CD18阳性细胞数显著增高,血浆LDL水平与CD11a、CD18阳性单个核细胞数明显相关,正常人单个核细胞经各因素处理后除内毒素对CD11b外其它被测细胞粘附分子阳性细胞数可升至病人水平,且冠心病患者单个核细胞之细胞粘附分子也以相同的反应性再度增高。结论单个核细胞表面CD11a、CD11b和CD18特别是CD11a和CD18的表达增强可能和动脉粥样硬化的发生有关。     

多发性骨髓瘤患者骨髓单个核细胞CUL4A表达及意义

目的检测多发性骨髓瘤(MM)患者骨髓单个核细胞中CUL4A mRNA表达,探讨其临床意义。方法采用实时荧光PCR相对定量法检测38例MM患者(MM组)和20例非血液肿瘤患者(对照组)骨髓单个核细胞CUL4A mRNA的表达情况。结果 MM组骨髓单个核细胞CUL4A mRNA相对表达量较对照组增加(P<0.05)。MM患者骨髓单个核细胞CUL4A mRNA相对表达量与临床分期、血清β2-MG水平相关(P均<0.05),与性别、年龄、免疫学分型不相关(P均>0.05)。治疗有效的MM患者骨髓单个核细胞CUL4A mRNA相对表达水平低于治疗无效患者(P=0.003)。结论 MM患者骨髓单个核细胞CUL4A mRNA表达上调可能是促进MM发展的因素之一,检测CUL4A可以为MM的诊断及治疗提供参考。     

粒细胞集落刺激因子动员对CD34^＋细胞黏附分子表达的影响

目的探讨粒细胞集落刺激因子（G—CSF）动员对CD34^＋细胞黏附分子表达的影响。方法应用流式细胞仪检测健康供者稳态及G—CSF动员过程中骨髓、外周血CD34^＋细胞的黏附分子表达变化，并应用结晶紫染色测定CD34^＋细胞的黏附功能。结果G-CSF动员后CD34^＋CD49d^＋细胞比例无显著下降，外周血CD34^＋CD621．^＋、CD34^＋CD54^＋和CD34^＋CDlla^＋细胞比例增高。动员后CD34^＋细胞表面CD49d的平均荧光强度显著减弱，但CD49e、CD62L、CDlla、CD54的平均荧光强度虽呈减弱趋势，却无统计学差异。动员后CD34^＋细胞黏附纤连蛋白能力下降。结论G—CSF通过降低造血干细胞与骨髓基质的黏附而产生动员效应。     

动脉粥样硬化患者CD_(11a)、CD_(11b)和CD_(18)表达的初步研究

目的　探讨动脉粥样硬化和白细胞功能相关抗原 (LFA 1即CD11a/CD18)以及巨噬细胞分化抗原 (Mac 1即CD11b/CD18)等细胞粘附分子表达的关系。方法　用碱磷酶抗碱磷酶 (A PAAP)桥联酶免疫细胞化学染色法检测冠心病患者外周血单个核细胞表面的CD11a、CD11b和CD18。结果　冠心病患者CD11a、CD11b、CD18阳性细胞数显著增高 ;血浆LDL水平与CD11a、CD18阳性单个核细胞数明显相关 ;正常人单个核细胞经各因素处理后除内毒素对CD11b外其它被测细胞粘附分子阳性细胞数可升至病人水平 ,且冠心病患者单个核细胞之细胞粘附分子也以相同的反应性再度增高。结论　单个核细胞表面CD11a、CD11b和CD18特别是CD11a和CD18的表达增强可能和动脉粥样硬化的发生有关     

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。     

共刺激分子CD28 CD152在类风湿关节炎患者T细胞亚群上表达异常的研究

目的观察共刺激分子CD28,CD152在类风湿关节炎(RA)患者的T细胞亚群上的表达异常情况,探讨RA的发病机制及治疗手段.方法用流式细胞仪采用直接免疫荧光法测定39例RA患者和20名健康对照人外周血T细胞表面标志CD3,CD4,CD8的表达情况及CD28,CD152在CD4+T和CD8+T细胞上的表达.结果 RA患者CD3+CD4+细胞较正常对照组显著增高(P＜0.01),CD3+CD8+细胞较正常对照组显著降低(P＜0.05),CD4+T细胞上CD28的表达较对照组显著降低(P＜0.05),而CD8+T细胞上CD28的表达与对照组差异无显著性(P＞0.05);CD4+T和CD8+T细胞上CD152的表达都较对照组显著增高(P＜0.01).结论在RA患者的细胞免疫活化过程中首先表现为B7/CD28信号途径占优势,T细胞被激活,激活的T细胞大量分泌CD152,它与CD28竞争结合B7分子,CD152/B7途径转而占优势,下调或终止T细胞反应.同时CD28+细胞数目的减少或功能缺陷造成RA患者外周血单个核细胞凋亡加速,是诱发RA患者的局部病理损害的原因.阻断CD152和B7的相互作用可增强特异性T细胞应答,为RA的免疫学治疗提供理论依据.     

CD4~+ CD25~(high) CD127~(low/-)调节性T细胞在多发性骨髓瘤患者外周血的表达

目的探讨多发性骨髓瘤(MM)患者外周血CD4+CD25highCD127low/-调节性T(Tregs)细胞表达水平及临床意义。方法采用流式细胞术(FCM)检测30例MM患者和20例健康对照者外周静脉血CD4+CD25highCD127low/-Tregs细胞水平。结果 1 MM组CD4+CD25high CD127low/-Tregs细胞表达明显高于正常对照组(P<0.05)。2MM组不同国际分期系统(ISS)分期CD4+CD25highCD127low/-Treg细胞水平均高于正常对照组,随着疾病进展,Ⅲ期明显高于Ⅱ期(P<0.05)。3MM组化疗后外周血CD4+CD25highCD127low/-Tregs细胞水平较化疗前显著下降(P<0.05)。结论 MM患者外周血CD4+CD25highCD127low/-Treg细胞比例明显升高,可能是MM免疫逃逸的一个重要机制;进展期Tregs的变化为MM患者及时进行临床干预提供实验依据。     

分化抑制培养体系体外扩增脐血造血细胞的研究

目的:探讨分化抑制培养体系对脐血造血细胞体外扩增效应。方法:分化抑制培养体系与脐血单个核细胞(MNC)体外共同培养7 d,检测MNC细胞总数、CFC、CD34 细胞反应扩增效果,并检测CD34 细胞表面归巢相关黏附分子VLA-4(CD49d)、VLA-5(CD49e)、LFA-1(CD11a)、HCAM(CD44)、L-selectin(CD62L)的表达率。结果:分化抑制培养体系组明显扩增脐血MNC细胞总数、CFC、CD34 细胞(均P<0．05),对照组培养脐血MNC细胞总数明显下降,CFC和CD34 细胞完全死亡(均P<0．01)。CD34 细胞表面各黏附分子CD49d、CD44和C1362L表达与扩增前相当(均P>0．05),而CD49e和CD11a表达明显高于扩增前(均P<0．05)。结论:分化抑制培养体系体外显著扩增脐血造血细胞,并且扩增后的造血干(祖)细胞总体上保持其表面归巢相关黏附分子的表达,归巢功能不会减低,是一种安全有效的扩增体系。     

高血压病与冠心病患者血小板表面CD41、CD62p的临床意义

目的 探讨血小板激活在高血压病与冠心病患者的意义。方法 测定正常人和高血压病与冠心病患者血小板表面CD41、CD62P,患者分成A、B、C三组,A组为未经抗血小板治疗的高血压病与冠心病患者37例,B组为正常对照组11例,C组为经抗血小板药治疗的高血压与冠心病患者28例。均取晨空腹静脉血3ml,用FACSCalibur流式细胞仪分析。结果A组CD41、CD41荧光强度和CD62p均高于B组(P<0.05),C组的CD41、CD41荧光强度、CD62p均低于A组(P<0.05)。高血压病组与冠心病组的相关指标比较无显著性差异。结论 高血压病与冠心病患者的血小板活化和激活增强,而抗血小板药物(阿司匹林或抵克立得)能抑制血小板激活。     

卡维地络对心绞痛患者白细胞表面CD11b及CD49d表达的影响

目的 :研究卡维地络对心绞痛患者外周血白细胞表面 CD11b及 CD49d表达的影响。方法 :住院冠心病患者共48（男 3 7,女 11）例 ,其中稳定型心绞痛 （SAP） 2 2例 ,不稳定型心绞痛 （UAP） 2 6例 ,随机将 SAP,U AP 2组患者 ,各分为治疗组 （给予卡维地络 10 m g口服 ,2 / d,术前 7d起使用 ）及对照组 （给予美托洛尔 12 .5 m g口服 ,2 / d,术前 7d起使用 ） ,分别于服药前及手术前采集股动脉血样 ,用 FCM直接免疫荧光法检测股动脉血中性粒细胞 （Neu）、单核细胞 （Mon）表面黏附分子 CD11b及 CD49d表达水平。结果 :服药前两组 CD11b及 CD49d表达均无显著差异 ,UAP患者卡维地络组与美托洛尔组 Neu与 Mon CD11b及 CD49d均高于 SAP患者组 （P <0 .0 5 ） ,服药 7d后UAP组 Neu CD11b卡维地络组明显低于美托洛尔组。结论 :不稳定心绞痛 Mon及 Neu CD11b及 CD49d表达均显著高于 SAP。卡维地络降低 Neu表面 CD11b及 CD49d表达 ,对 Mon的影响尚有待评估     

Granulocyte-colony stimulating factor increases CD123hi blood dendritic cells with altered CD62L and CCR7 expression

Changes in blood dendritic cell (BDC) counts (CD123(hi)BDC and CD11c(+)BDC) and expression of CD62L, CCR7, and CD49d were analyzed in healthy donors, multiple myeloma (MM), and non-Hodgkin lymphoma (NHL) patients, who received granulocyte-colony stimulating factor (G-CSF) containing peripheral blood stem cell (PBSC) mobilization protocols. Low-dose G-CSF in healthy donors (8-10 microg/kg/d subcutaneously) and high-dose G-CSF in patients (30 microg/kg/d) increased CD123(hi)BDC (2- to 22-fold, mean 3.7 x 10(6)/L-17.7 x 10(6)/L and 1.9 x 10(6)/L-12.0 x 10(6)/L) in healthy donors and MM but decreased CD11c(+)BDC (2- to 10-fold, mean 5.7 x 10(6)/L-1.6 x 10(6)/L) in NHL patients, on the day of apheresis, compared with steady state. After apheresis, CD123(hi)BDC counts remained high, whereas low CD11c(+)BDC counts tended to recover in the following 2-5 days. Down-regulation of CD62L and up-regulation of CCR7 on CD123(hi)BDC were found in most healthy donors and MM patients. CD49d expression was unchanged. Thus, PBSC mobilization may change BDC counts by altering molecules necessary for BDC homing from blood into tissues.     

心绞痛患者单核细胞粘附分子和细胞因子的变化

目的　观察不稳定心绞痛患者外周血单核细胞粘附分子表达和分泌细胞因子的变化 ,并探讨其临床意义。方法　以接受常规冠状动脉造影的 42名患者为研究对象 ,根据临床诊断将有明显冠状动脉疾病的冠心病患者分为不稳定心绞痛和稳定劳力心绞痛两组 ,而以冠状动脉正常的为对照组 ;体外分离单核细胞 ,用流式细胞仪直接免疫荧光法检测单核细胞膜表面CD1 1b、CD49d和CD54表达 ,并应用放射免疫及ELISA法检测其分泌TNF α ,IL 8的情况。结果　不稳定心绞痛及稳定劳力心绞痛两组单核细胞膜表面CD1 1b ,CD49d和CD54表达及TNF α ,IL 8分泌明显高于对照组 (P <0 .0 1 ) ,其中不稳定心绞痛组又高于稳定劳力心绞痛组 (P <0 .0 5) ;冠状动脉狭窄程度和病变支数与单核细胞膜表面CD1 1b、CD49d和CD54表达及TNF α,IL 8的分泌无明显相关。结论　冠心病患者循环血存在单核细胞激活现象 ,其活性与冠状动脉病变程度无关 ,提示循环血单核细胞的激活在不稳定心绞痛病理发生中起重要作用     

Expression of HLA-DR, CAM and co-stimulatory molecules on cord blood monocytes

Umbilical cord blood (CB) transplantations are associated with a lower risk of severe graft-versus-host disease (GVHD) compared to BMT. GVHD is an immune reaction that involves interaction between cell surface molecules resulting in cell activation and release of many cytokines. Monocytes are known to be an important source of cell adhesion (CAM) and co-stimulatory molecules which play a crucial role in the efficient activation of T and B cells. We analyzed the phenotype of CB monocytes in the presence or absence of an inflammatory signal (rIFN-gamma) and compared them to adult blood (AB); the expression of HLA-DR and 17 different markers (CD11a, CD11b, CD11c, CD18, CD29, CD40, CD44, CD49a, CD49d, CD49e, CD49f, CD54, CD58, CD62L, CD80, CD86 and CD102) was measured by flow cytometry. Statistical analysis showed that, compared to AB, CB monocytes did not express CD11b, CD11c, CD49d and after stimulation with rIFNgamma, they lost the expression of CD58 and CD102, whereas CD80 and CD86 expression was induced. The analysis of fluorescence intensity (MFI) revealed that CB monocytes expressed some CAM (CD29, CD54, CD102) with a lower intensity than AB monocytes except CD44. In conclusion, absence and reduced expression of some markers argue for a different phenotypic profile of CB monocytes compared to AB monocytes, which might partly contribute to their impaired immune response and to the low incidence of GVHD observed after CB transplantations. However, CB monocytes expressed CD80 and CD86 co-stimulatory molecules, but this expression did not prove a normal co-stimulatory function.     

CD11b/CD18在心肌梗死患者室内空气净化前、后的表达

目的：探讨老年陈旧性心肌梗死息空气净化前、后中性粒细胞和单核细胞膜CD11b／CDl8的表达。方法：老年陈旧性心肌梗死(OMI)疗养员141例随机分为空气净化组(n＝75)和未净化组(n＝66)，另选20人为健康对照组。空气净化组所处的疗养室进行24小时空气净化，未净化组位普通病房，不进工空气净化。住院时和住院后每隔1个月抽血，应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／CDl8的表达。结果：空气净化1个月后，症状心电图总有效率分别为93％、79％，显好于未净化组的45％、44％(P＜0．01)。思考的中性粒细胞和单核细胞膜CDllb／CD，e的表达较净化前显降低，亦低于非净化组，但高于正常对照组；P均＜0．01。结论：对OMI息进行空气净化治疗，有益于改善其中性粒细胞和单核细胞膜CDlIb／CD18的表达。     

In vivo and in vitro expression of adhesion molecules by peripheral blood lymphocytes from patients with primary Sjogren's syndrome: culture-associated enhancement of LECAM-1 and CD44

The interaction of adhesion receptors on lymphocytes with their ligands over endothelial cells provides the mechanism by which lymphocytes infiltrate target tissues in autoimmune diseases. Primary Sjogren's syndrome (SS) is associated with lymphocytic infiltration in exocrine glands. The aim of this study was to examine levels of expression of adhesion molecules by peripheral blood lymphocytes from patients with SS (before and after stimulation). Peripheral blood lymphocytes from 16 patients with primary SS and from 15 controls were stained directly or cultured for 72 h with and without phytohaemagglutinin (PHA). Indirect immunofluorescence with monoclonal antibodies and flow cytometry were used. The following molecules were detected in patients before culture: CD18 (mean percentage 94%), CD11a (94%), CD11b (39%), CD54 (23%), CD58 (62%), CD44 (Hermes-1; 82%), CD49-d (VLA-4; 80%), CD25 (11%) and LECAM-1 (62%). After stimulation with PHA, there was an increase in the levels of CD18 (2.5-fold), CD11a (2.3-fold), CD54 (10.2-fold), CD58 (2.5-fold), CD44 (2.4-fold), CD49d (3.4-fold) and CD25 (62-fold) on lymphocytes from both patients and controls. The number of positive cells and level of expression did not differ from the controls, except in the case of unstimulated, cultured lymphocytes in which the levels of CD44 and LECAM-1 were increased more in patients than in normal controls. The increase in the level of in vitro expression of CD44 (P< 0.05) and LECAM-1 (P< 0.002) on lymphocytes from patients with primary SS reached statistical significance when compared to similarly cultured lymphocytes from controls. The regulation of LECAM-1 and CD44 expression in patients with SS may contribute to the immunopathogenesis of this desease by increased tethering or rolling (early adhesive events) of lymphocytes over endothelial cells. Such molecules may be involved in lymphocytic homing to tissues in SS.     

Multiple myeloma: altered CD4/CD8 ratio in bone marrow

The expression of CD3, CD4 and CD8 antigens was simultaneously evaluated in peripheral blood and bone marrow lymphocytes from 22 multiple myeloma (MM) patients. The coexpression of CD11b and HLA-DR antigens was also analyzed within the CD4+ and CD8+ subpopulations in 4 MM patients. In peripheral blood the percentage of CD3+ and CD8+ cells was in the normal range, and the percentage of CD4+ was slightly reduced, leading to an altered CD4/CD8 ratio (less than 1) in only 7 patients. On the contrary, in bone marrow the percentage of CD4+ was profoundly reduced, leading to an altered CD4/CD8 ratio in all MM patients. As we previously reported in peripheral blood, an expansion of the CD11b+ and HLA-DR+ lymphocytes was observed within the CD4+ and CD8+ bone marrow T-cell subpopulations. A T-lymphocyte subset imbalance is more evident in bone marrow than in peripheral blood, and it is not due to a different lymphocyte distribution within the hematological compartments.