白细胞介素－6和肿瘤坏死因子调节冠心病患者单个核粒细胞CD116抗原表达

白细胞介素－６和肿瘤坏死因子调节冠心病患者单个核粒细胞ＣＤ_（１１６）抗原表达安靓，李进，刘小荣（广州第一军医大学细胞生物学实验室，５１０５１５）ＣＤ１１６是近年来广受重视的白细胞表面粘附受体家族的成员，可介导白细胞与血管内皮细胞的粘附，并可能与动脉?..     

狼疮性肾炎患者CD^＋淋巴细胞减少机制的初步探讨

目的：探讨ＣＤ９５表达在狼疮性肾炎（ＬＮ）患者ＣＤ４＾＋淋巴细胞和中所起的作用。方法：采用ＣＤ４＋ＣＤ９５双荧光标记及ＣＤ４＾＋细胞的原位杂交ＤＮＡ链断端标记,结合流式细胞术和ＤＮＡ琼脂糖电泳对ＬＮ患者中血单个核的免疫分型及凋亡特征进行分析。结果：（１）ＬＮ虱较正常人ＣＤ４＾＋细胞比例明显减少（Ｐ〈０．０１）,ＣＤ８＾＋细胞比例明显升高（Ｐ〈０．０１）。（２）ＬＮ患者ＣＤ４＾＋细胞有５１．２％表达     

慢性髓细胞性白血病病程进展中调节蛋白c—Myc,Bcl—2ey Fas的表？…

目的 了解细胞程序死亡（ＰＣＤ）与慢性细胞性白血病（ＣＭＬ）急变的关系。方法 采用流式细胞术，测定２１例ＣＭＬ及１２例正常骨髓标本单个核细胞的髓系免疫表型及三种与ＰＣＤ有关的调节蛋白－ｃ－Ｍｙｃ、Ｂｃｌ－２、Ｆａｓ的表达。结果 与未治慢性期比较，加速／急变期膜抗原最显著的变化是ＨＬＡ－ＤＲ％的提高，ＣＤ１５％ＨＬＡ－ＤＲ％比值倒置。正常骨髓及ＣＭＬ各期ＨＬＡ－ＤＲ及ＨＬＡ＿ＤＲ细胞几乎均表达ｃ－ｍ     

纤维蛋白原样蛋白2在急性冠状动脉综合征患者外周血单个核细胞中的表达和意义

目的:探讨纤维蛋白原样蛋白2(fgl2)在急性冠状动脉综合征(ACS)患者外周血单个核细胞中的表达及其意义.方法:用荧光定量PCR法检测60例ACS、25例稳定型心绞痛(SA)患者和20例正常人外周血中单个核细胞中fgl2的表达量水平.结果:ACS组fgl2基因表达明显高于SA组和正常对照组(均P<0.05),SA组与正常对照组比较差异无统计学意义(P>0.05).结论:ACS患者急性期外周血单个核细胞中fgl2的表达明显增加, 可能是ACS微循环障碍有预测价值的急性时相性蛋白之一.     

细胞因子对冠心病患者单核细胞粘附相关蛋白表达的调节

为研究白细胞介素-1、肿瘤坏死因子、白细胞介素-6和α-干扰素等细胞因子对冠心病单核细胞粘附相关蛋白表达的调节作用，采用免疫组织化学法显示白细胞分化抗原CD11b、CD44和体外连接蛋白Vn在单个核细胞表面的分布，用图像分析仪进行定量，并用统计学析因分析的方法对实验结果进行多因素的分析。结果显示，CD11b、CD44和Vn阳性区域为粉红至桃红色，多呈环状、半月状、帽状、斑片状及颗粒状，三种抗原在细胞表面的分布不同。图像分析结果显示白细胞介素-1、肿瘤坏死因子和白细胞介素-6作用后CD11b、CD44和Vn的表达增加，其中冠心病患者较对照组增加更加明显（P＜0．001），α-干扰素的作用不明显。以上提示，冠心病时白细胞介素-1、肿瘤坏死因子和白细胞介素-6对粘附相关蛋白表达的上调作用明显增强，表明冠心病人粘附蛋白表达对某些细胞因子的敏感性升高，细胞因子可通过调节单核细胞表面粘附相关蛋白的表达，而影响单核细胞与内皮细胞的粘附，进而影响动脉粥样硬化的病变过程。     

肺结核患者外周血单个核细胞CD23,CD40表达过程中PPD的影响作用

肺结核患者外周血单个核细胞ＣＤ２３、ＣＤ４０表达过程中ＰＰＤ的影响作用王珂黄瑾李淑芳为继续对精制蛋白衍化物（ＰＰＤ）在ＣＤ２３、ＣＤ４０表达过程中的影响作用作进一步研究，期望为说明结核患者机体免疫功能状态提供依据，１９９５年９月～１９９６年４月对我院...     

哮喘患者细胞粘附分子表达及血浆可溶性E-选择素、P-选择素含量变化研究

哮喘患者细胞粘附分子表达及血浆可溶性Ｅ－选择素、Ｐ－选择素含量变化研究张波刘树芬张劭夫齐法莲孙文杰细胞粘附分子与哮喘气道粘膜炎性细胞浸润有密切关系［１］，本组对哮喘患者外周血单个核细胞（ＰＢＭＣｓ）表面的ＣＤ１１ａ／ＣＤ１８（淋巴细胞功能相关抗原－１...     

扩张型心肌病白细胞介素2受体的初步研究

检测２０例扩张型心肌病（ＤＣＭ）及２０例正常人（ＮＣ）的血清可溶性白细胞介素２受体（ＳＩＬ－２Ｒ）及外周血单个核细胞膜白细胞介素２受体（ＩＬ－２Ｒ）的表达。结果发现，ＤＣＭ患者ＳＩＬ－２Ｒ明显高于ＮＣ组（Ｐ＜０．００１），而膜ＩＬ－２Ｒ表达低于ＮＣ组（Ｐ＜０．０１），提示ＩＬ－２Ｒ在ＤＣＭ发病中可能有一定意义。     

慢性髓细胞性白血病病程进展中调节蛋白c-Myc、Bcl-2及Fas的表达变化

目的了解细胞程序死亡（ＰＣＤ）与慢性髓细胞性白血病（ＣＭＬ）急变的关系。方法采用流式细胞术，测定２１例ＣＭＬ及１２例正常骨髓标本单个核细胞的髓系免疫表型及三种与ＰＣＤ有关的调节蛋白——ｃ－Ｍｙｃ、Ｂｃｌ－２、Ｆａｓ的表达。结果与未治慢性期比较，加速／急变期膜抗原最显著的变化是ＨＬＡ－ＤＲ＋％的提高，ＣＤ＋１５％／ＨＬＡ－ＤＲ＋％比值倒置。正常骨髓及ＣＭＬ各期ＨＬＡ－ＤＲ＋及ＨＬＡ－ＤＲ－细胞几乎均表达ｃ－Ｍｙｃ，差别只在于表达量的多少，未治慢性期与正常骨髓组相似，加速／急变期组不仅显著高于未治慢性期组，其ＨＬＡ－ＤＲ＋细胞群的ｃ－Ｍｙｃ表达量亦显著高于正常骨髓组。Ｂｃｌ－２＋％在未治慢性期低于正常骨髓，加速／急变期组显著提高。Ｆａｓ在ＣＭＬ各期及正常骨髓均为低表达。结论处于未治慢性期的中、晚幼粒细胞的大量聚集似乎与Ｂｃｌ－２、Ｆａｓ的ＰＣＤ调节作用无关；而在加速／急变期组尤其是造血祖细胞不仅有增殖过旺，亦存在ＰＣＤ受阻     

重组人干细胞因子促进正常人早期造血功能

重组人干细胞因子促进正常人早期造血功能唐继森，王辨明，李崇渔，马军干细胞因子是９０年代新发现的造血生长因子。我们报道基因重组产品重组人干细胞因子（ｒｈＳＣＦ）对正常人早期造血功能的作用。材料和方法（１）研究对象和骨髓去粘附细胞、去Ｔ淋巴细胞的单个核细...     

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。     

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     

外周血单个核细胞表面CD44表达水平与冠心病及其严重程度有关联

目的:观察不同类型冠心病患者外周血单个核细胞(PBMC)表面CD44的表达变化情况,并探讨其临床意义。方法:采用实时荧光定量RT-PCR法,对正常对照30例,稳定型心绞痛(SAP)26例,不稳定型心绞痛(UAP)29例、急性心肌梗死(AMI)27例的PBMC表面CD44 mRNA进行检测,并以β-actin作为内参进行半定量评价。结果:1UAP和AMI组PBMC表面CD44 mRNA水平均显著高于SAP组和正常对照组(P0.05);2AMI组PBMC表面CD44 mRNA水平显著高于UAP组(P0.05);3SAP组与正常对照组相比,PBMC表面CD44 mRNA水平无统计学差异。结论:PBMC表面CD44表达的水平与冠心病及其病情的严重程度有关联。     

Expression of leukocyte adhesion molecules by mucosal mononuclear phagocytes in inflammatory bowel disease.

Leukocyte adhesion molecules are important in cell-cell interactions of the immune system. Lymphocyte function-associated antigen 1 (cluster designation 11a) mediates interactions between T cells and mononuclear phagocytes through its ligand, the intercellular adhesion molecule 1 (CD54), whereas complement receptors 3 (CD 11b) and 4 (CD11c) are involved in complement-mediated phagocytosis. Expression of CD11 molecules and intercellular adhesion molecule 1 was studied in colonic biopsy specimens from 20 patients with inflammatory bowel disease and 10 normal controls. In normal colon, few mononuclear phagocytes expressed lymphocyte function-associated antigen 1 and intercellular adhesion molecule 1 at high densities. The major adhesion molecule was CD11c. Thus, the largest population of normal colonic mononuclear phagocytes was represented by quiescent, resident macrophages with likely phagocytic function. In inflammatory bowel disease, mononuclear phagocytes showed only a slight increase in CD11a expression and no significant change in expression of CD11b and CD11c. By contrast, the percentage of mononuclear phagocytes expressing intercellular adhesion molecule 1 was increased from 6.9% +/- 3.9% in controls to 69.2% +/- 12.8% in ulcerative colitis (P less than 0.001) and to 45.7% +/- 22.8% in Crohn's disease (P less than 0.01), showing a close relationship with histological activity. The increased expression of intercellular adhesion molecule 1 in inflammatory bowel disease indicates a state of immunological activation induced by local release of inflammatory cytokines. Such induction of intercellular adhesion molecule 1 on mononuclear phagocytes may be important in the maintenance of chronic inflammation by facilitating interactions with T cells and T-cell antigen recognition.     

Expression of the CD11/CD18, leukocyte adhesion molecule 1, and CD44 adhesion molecules during normal myeloid and erythroid differentiation in humans.

We have used three-color flow cytometry to investigate the pattern of expression of the CD11/CD18, CD44, and leukocyte adhesion molecule 1 (LAM-1) adhesion molecules during myeloid and erythroid differentiation in humans. The earliest myeloid cells, identified as CD33loCD15-, were exclusively CD44hi but contained both leukocyte function-associated antigen 1 (LFA-1hi) and LFA-1lo cells, as well as LAM-1+ and LAM-1- cells. This CD33loCD15- myeloid subpopulation expressed only low levels of CD11c and failed to express CD11b, CD14, or any lymphoid (CD3, CD16, CD19) antigens or glycophorin. Commitment to monocyte differentiation, suggested by the presence of an LFA-1hi CD11c+ subset within the CD33loCD15- subpopulation, was clearly signaled by upregulation of CD33; these monocyte-lineage committed cells were exclusively CD33hi, CD44hi, CD11ahi, CD11c+, and exhibited a broad range of intensity of CD15 expression. Later stages of monopoiesis were identified by acquisition of CD11b, and subsequently of CD14. Myeloid cells committed to granulopoiesis remained LFA-1lo, and underwent a sharp upregulation of CD15 along with downregulation of both CD33 and CD44. Successive stages of granulocyte development were marked by expression of CD11b and, subsequently, of CD16. The earliest cells capable of erythroid differentiation were CD44hi, LFA-1lo, and LAM-1+. Both LFA-1 and LAM-1 were lost before the onset of glycophorin (glyco) expression, whereas CD44 expression remained high on glyco+ cells, which also expressed CD45. CD44 expression was intermediate on glyco+ CD71+ cells, and low on glyco+ CD45- CD71- cells, similar to normal, circulating erythrocytes. Our results allow us to phenotypically define discrete stages in the normal development of monocytes, neutrophils, and erythrocytes. The expression of LFA-1, LAM-1, and high levels of CD44 on the most primitive hematopoietic cells detectable by flow cytometry suggests that at least some of these molecules are critically involved in leukocyte adhesion during development.     

Phenotypic analyses and concanavalin-A-induced suppressor cell dysfunction of intrathyroidal lymphocytes from patients with Graves' disease

The expression of phenotypic markers and Concanavalin-A-induced suppressor activity was compared among mononuclear cells isolated from thyroid glands and peripheral blood of thionamide-treated patients with hyperthyroid Graves' disease and peripheral blood from normal subjects. Intrathyroidal lymphocytes were obtained by two different methods (TG-1 and TG-2 cells), gradient centrifugation of supernatants of minced thyroid tissue and overnight culture of thyroid debris after mechanical disaggregation and enzymatic digestion, respectively. The percentages of CD3+ cells (all mature T cells) among peripheral blood and TG-1 and TG-2 cells from Graves' patients were similar, but the percentages of B1+ cells (pan B cells) among the TG-1 and TG-2 cells were markedly increased compared to that in peripheral blood. The percentages of CD4+ cells among the TG-1 and TG-2 cells were significantly less than that in peripheral blood. The percentages of CD4+2H4+ cells among CD4+ cells in TG-1 and TG-2 cells also were significantly less than that in peripheral blood. The percentage of CD4+4B4+ cells among CD4+ cells in thyroid glands was markedly higher than that in peripheral blood. The percentages of CD8+ cells and CD8+CD11b- cells (cytotoxic T cells) in thyroid glands were significantly higher than those in peripheral blood from Graves' patients and peripheral blood from normal subjects. The CD8+CD11b+ cells were subdivided into two subpopulations on the basis of CD8 antigen density. The percentage of dull CD8+CD11b+ cells (natural killer cells) among TG-2 cells was lower than that in peripheral blood, but there was no significant difference in bright CD8+CD11b+ cells (suppressor-effector T cells) between thyroid glands and peripheral blood. The percent suppression induced by Concanavalin-A in both TG-1 and TG-2 cells was significantly decreased compared with that in peripheral blood. These results suggest that impairment of suppressor cell activity and an increased number of B cells exist in thyroid glands of patients with Graves' disease compared to those in peripheral blood. It, thus, appears likely that both B cell hyperactivity and suppressor T cell dysfunction may induce excess production of autoantibodies in the thyroid glands of such patients.     

普伐他汀对冠心病患者外周血单核细胞功能的影响

为探讨普伐他汀对冠心病患者外周血单核细胞（ＰＢＭｓ）功能的影响,对２１例血脂正常冠心病患者和９例健康人ＰＢＭｓ粘附分子ＣＤ１１ｂ、ＣＤ４９ｄ表达及ＴＮＦ－α、ＩＬ－８分泌情况进行了检测;并在体外分离培养的冠心病患者ＰＢＭｓ中,观察了普伐他汀对其表达ＣＤ１１ｂ、ＣＤ４９ｄ及分泌ＴＮＦ－α、ＩＬ－８的影响。结果表明：冠心病患者ＰＢＭｓ表达ＣＤ１１ｂ、ＣＤ４９ｄ及分泌ＩＮＦ－α、ＩＬ－８的能力明显高于正常对照组（Ｐ＜００１）;普伐他汀能下调冠心病患者ＰＢＭｓＣＤ１１ｂ、ＣＤ４９ｄ表达及降低ＴＮＦ－α、ＩＬ－８的分泌（Ｐ＜００５）。说明普伐他汀可抑制冠心病患者外周血单核细胞的功能。     

Lymphokine production by T-cell clones after human bone marrow transplantation

T cells recovering after bone marrow transplantation (BMT) were analyzed for their phenotypic and functional features by two-color immunofluorescence and a high efficiency cloning technique. A predominance of cells co-expressing natural killer (NK)-related surface antigens, such as Leu 7 (CD57) and CD11b, was detected within both the CD4+ and CD8+ subsets from 5 months postgrafting onward. Such cells are virtually absent among normal circulating CD4+ cells and account for a minority (approximately 30%) of normal CD8+ cells. Postgrafting T cells representative of the whole range of NK-related antigen co-expression were selected from six patients for clonal analyses. In control subjects, 63% and 41% of the CD4+ and CD8+ clones, respectively, produced interleukin-2 (IL-2) whereas approximately 30% of either CD4+ or CD8+ control clones produced interferon (IFN)-gamma. At variance, and irrespective of their CD4+/CD8+ phenotype, lower proportions of BMT recipient-derived clones produced IL-2 (20% and 12%, respectively), whereas the majority of both CD4+ and CD8+ clones (75% and 71%, respectively) released high amounts of IFN-gamma. Purified populations of CD57+/CD11b+ v negative cells from two BMT recipients and two control subjects were cloned and subsequently evaluated for IL-2 and IFN-gamma production. CD57+/CD11b+ cell-derived clones were poor IL-2 producers in both normal subjects and BMT patients. In contrast, IL-2-producing clones were frequent (62% to 79%) among those derived from CD57-/CD11b- cells from normal subjects, whereas they were still represented at lower than normal proportions, ie, 25% to 41%, among clones generated from BMT recipients. CD57+/CD11b+ cells gave rise to comparably high proportions of IFN-gamma producing clones in both normal subjects and BMT recipients (approximately 80%). In contrast, IFN-gamma producing clones were approximately 25% to 50% of CD57-/CD11b- cell-derived clones in both normal subjects and BMT patients. Therefore, while the predominance of NK-related antigen-positive T cells may be predictive of poor IL-2 and high IFN-gamma production, the immune derangement in long-term BMT recipients is further enhanced by the finding that all T cells may be poor IL-2 producers. It is also suggested that IL-2 production is a preferential function of T cells that do not express CD57 and CD11b, whereas IFN-gamma production is attributable to T cells that express CD57 and CD11b.