八种粘附分子在急性淋巴细胞性白血病异常表达的研究

本文分析了３８名正常人和２５例急性淋巴细胞性白血病（ＡＬＬ）细胞表面ＣＤ１１ａ、ＣＤ１１ｂ、ＣＤ５４、ＣＤ４４等的表达。与正常人相比，肿瘤细胞上表达的ＣＤ１１ｂ、ＣＤ１８和ＣＤ５４降低，ＣＤ４４升高；ＣＤ１１ａ在Ｂ－ＡＬＬ和混合型ＡＬＬ表达减弱，在Ｔ－ＡＬＬ增强。３例急性淋巴细胞性白血病骨髓基质细胞表面ＣＤ５４、ＣＤｗ４９ｂ表达亦降低。认为粘附分子可能参与了急性淋巴细胞性白血病的发病机制。     

缺血预适应阻抑犬冠状窦血中性粒细胞CD11b/CD18的表达

本文旨在探讨缺血预适应（ＩＰ）心肌保护效应是否与其防止中性粒细胞（ＰＭＮ）ＣＤ１１ｂ／ＣＤ１８分子的表达有关。采用犬衣降支动脉（ＬＡＤ）建立ＩＰ模型,在长缺血前各５ｍｉｎ血和再灌注,反复４次,于基础、缺血前、缺血１ｈ、再灌注０．５和２ｈ分别采集冠状窦血作式细胞仪分析ＰＭＮＣＶＤ１１ＣＤ１８的表达,并一单纯ＩＲ组比较。ＩＲ组在心肌缺因与再灌注各时点ＰＭＮＣＤ１１ｂ／ＣＤ１８表达均显著增加,而ＩＰ组除     

急性淋巴细胞性白血病细胞及其骨髓基质细胞粘附分子表达和粘附行为的探讨

分析了５８例急性淋巴细胞性白血病（ＡＬＬ）患者和１０例正常人骨髓单个核细胞及其骨髓基质细胞上粘附分子的表达。发现与正常人相比，白血病细胞上表达的ＣＤ１１ａ、ＣＤ１１ｂ、ＣＤ１８、ＣＤ３４、ＣＤ４４、ＣＤ４９ｄ和基质细胞上表达的ＣＤ５４，ＣＤ４９ｂ均有显著性改变（明显下降或显著增高）；同时，来自ＡＬＬ的基质细胞在粘附分子表达和粘附行为上亦不同于正常骨髓基质细胞，认为粘附分子的异常表达可能参与了ＡＬＬ的发病机制。     

TNFα对人外周血CD15^＋细胞表面粘附分子的诱生及氨茶碱的作用

目的和方法：应用双色免疫荧光流式细胞技术观察了肿瘤坏死因子（ＴＮＦα）对人外周血中性粒细胞（ＣＤ１５＋细胞）粘附分子ＣＤ１１α、ＣＤ１１ｂ、ＣＤ４９ｄ和ＣＤ６２Ｌ的诱生作用和氨茶碱对其影响。结果：不同浓度的ＴＮＦα可诱导中性粒细胞ＣＤ１１ａ和ＣＤ６２Ｌ的表达，对ＣＤ１１ｂ和ＣＤ４９ｄ无明显作用。不同剂量的氨茶碱对粘附分子的表达有一定作用。氨茶碱在７５ｍｇ／Ｌ浓度时增强ＣＤ１１ａ和ＣＤ６２Ｌ的表达；１２５ｍｇ／Ｌ时抑制其表达；２５０ｍｇ／Ｌ时抑制ＣＤ６２Ｌ的表达，对ＣＤ１１ａ无明显作用。结论：ＴＮＦα可调节中性粒细胞表面某些粘附分子的表达，氨茶碱对粘附分子的作用在临床应用上具有一定的指导意义。     

IL-10对U937细胞CD14、CD11b、CD23和HLA-DR表达的影响

Ｋ２〗ＩＬ１０是１９８９年Ｆｉｏｒｅｎｔｉｎｏ等首先发现的一种免疫负调因子,由Ｔｈ２细胞产生,可抑制Ｔｈ１细胞产生ＩＦＮγ［１］。又发现它对单核巨噬细胞、Ｔ细胞、ＮＫ细胞和Ｂ细胞等都有免疫调节作用,但ＩＬ１０对原始细胞免疫调节的研究还很少。Ｕ９３７细胞是一种人原始单核系白血病细胞,代表了单核细胞分化的早期阶段［２］。本文观察了ＩＬ１０对Ｕ９３７细胞固有和ＩＦＮγ诱导下ＣＤ１４、ＣＤ１１ｂ、ＣＤ２３和ＨＬＡＤＲ表达的影响。１　材料和方法１－１　细胞系　人原始单核系Ｕ９３７细胞在含１０％…     

慢性支气管炎患者肺泡巨噬细胞上CD11c、CD14及？…

目的 研究慢性支气管炎患者肺泡巨噬细胞上ＣＤ１１ｃ和ＣＤ１４及其胞内ＴＧＦ－β１ｍＲＮＡ的表达情况。方法 对慢性支气管炎缓解期患者和正常对照者各１０例进行局部支气管肺泡灌洗。将支气管肺泡灌洗涤液中的肺泡巨噬细胞分离、纯化后，与藻红蛋白（ｐｈｙｃｏｅｒｙｔｈｒｉｎ，ＰＥ）和异硫氰酸荧光素（ｆｌｕｏｒｅｓｃｅｉｎ ｉｓｏｔｈｉｏｃｙａｎａｔｅ，ＲＩＴＣ）标记的ＣＤ１１ｃ和ＣＤ１４单克隆抗体共同孵育，以     

SLE患者细胞粘附分子CD11a、CD18、CD54表达初探

利用流式细胞术及免疫荧光双染色法，检测３５例系统性红斑狼疮（ＳＬＥ）患者外周血细胞粘附分子表型（ＣＤ１１ａ、ＣＤ１８、ＣＤ５４）及淋巴细胞表型（ＣＤ３、ＣＤ４、ＣＤ８、ＣＤ４５、ＲＡ、ＣＤ４５ＲＯ）。结果表明，ＳＬＥ活动组ＣＤ８＋细胞增高，ＣＤ４＋ＣＤ４５ＲＡ＋细胞减少；ＣＤ４＋细胞表面ＣＤ１１ａ、ＣＤ１８表达降低，后二者在ＣＤ８＋细胞上表达增高；ＣＤ５４在ＣＤ２０＋细胞上增高。进一步发现，ＣＤ８＋细胞的ＣＤ１８增高与ＣＤ４＋ＣＤ４５ＲＡ＋细胞减少呈负相关（Ｐ＜００５），而与ＣＤ２０＋细胞表面ＣＤ５４增高呈正相关（Ｐ＜００１）。本文提示，细胞粘附分子可能在ＳＬＥ发病机理中占有重要意义。     

CD40和CD40配体的研究进展

ＣＤ４０是一种存在于Ｂ淋巴细胞、树突状细胞、造血前体细胞、上皮细胞及某些癌细胞表面的跨膜糖蛋白。由２７７个氨基酸组成，分子量为４５～５０ＫＤａ，是ＴＮＦ－Ｒ超家族成员。人ＣＤ４０基因定位于２０号染色体ｑ１１－３，小鼠基因位于２号染色体上。ＣＤ４０配体（ＣＤ４０Ｌ）由２６１个氨基酸构成，分子量为３４ＫＤａ，是ＴＮＦ超家族成员。基因位于ｘｑ２４。主要存在于活化的ＣＤ４＋Ｔ细胞表面，在ＣＤ８＋、嗜碱／肥大细胞表面也有表达。ＣＤ４０与ＣＤ４０Ｌ间的反应与Ｂ细胞活化、增殖、抗体的产生、生发中心的形成有关。反应的中断可导致免疫耐受，ＣＤ４０Ｌ缺陷可造成性联高ＩｇＭ综合征（ＨＩＭ）。     

粘附分子对CD3介导的胸腺细胞[Ca^2＋]i应答的影响

ＬＦＡ－１和ＩＣＡＭ－１广泛表达于各胸腺细胞亚群，但ＩＣＡＭ－１在ＰＮＡ￣＋细胞的表达下调。本文报道：用抗ＬＦＡ－１／ＩＣＡＭ－１和抗ＣＤ３单抗，分析了粘附分子ＬＦＡ－１／ＩＣＡＭ－１对抗ＣＤ３诱导的胸腺细胞［Ｃａ￣（２＋）］ｉ应答的影响。结果显示，可溶性抗ＬＦＡ－１／ＩＣＡＭ－１可抑制ＣｏｎＡ刺激的胸腺细胞增殖，且以抗ＬＦＡ－１抗体的作用更为显著，在ＣｏｎＡ或抗ＣＤ３诱导的胸腺细胞［Ｃａ￣（２＋）］ｉ应答中，抗ＬＦＡ－１单抗可明显抑制［Ｃａ￣（２＋）ｉ升高。但如果用二抗交联ＣＤ３和ＬＦＡ－１，胸腺细胞［Ｃａ￣（２＋）ｉ则显著高于单独交联ＣＤ３时的水平（Ｐ＜０．０１），而ＣＤ３与ＩＣＡＭ－ｌ交联却无此效应，此外，仅交联ＬＦＡ－１或ＩＣＡＭ－１也无诱导［Ｃａ￣（２＋）］ｉ应答的作用。提示在ＬＦＡ－ｌ与ＩＣＡＭ－１介导的胸腺细胞与胸腺基质细胞相互作用中，ＬＦＡ－１可为ＴＣＲ／ＣＤ３途径介导的胸腺细胞活化提供复合刺激信号。     

人创伤性休克时白细胞表面LFA-1、Mac-1、CD18的表达

探讨人创伤性休克时白细胞表面ＬＦＡ－１、Ｍａc－１和ＣＤ１８表达变化。方法：间接免疫荧光标记法。结果：创伤性休克后多形核粒细胞（ＰＭＮｓ）表面ＬＦＡ－１、Ｍａｃ－１和ＣＤ１８表达呈下降趋势,但无显著意义（Ｐ＞０．０５）。单核细胞表面ＬＦＡ－１、Ｍａｃ－１和ＣＤ１８表达呈上升趋势,以ＣＤ１８为显著（Ｐ<０．０５）。结论：创伤后ＰＭＮｓ表面粘附分子表达量与它对内皮的粘附存在不一致性,而单核细胞粘附也似乎不仅仅依赖于粘附分子的表面受体表达增强。提示,单核细胞与ＰＭＮｓ在参与粘附反应时其表面ＣＤ１８表达量变化不一致,其功能调节是否一致尚待查明。     

整合素CD11a、CD11b和CD11c在大鼠心脏发育中的表达变化

目的 探讨整合素CD11a、CD11b和CD11c在大鼠心脏发育中的表达变化。方法 利用免疫组织化学和RT-PCR方法,检测胚胎18d(E18d)、生后5d(P5d)、P19d、P40d及生后1年（P1y）大鼠心肌组织的CD11a、CD11b和CD11c的基因和蛋白表达。结果 免疫组织化学结果显示,大鼠心肌
组织CD11a、CD11b和CD11c表达部位在心肌细胞质内;从E18d到P1y大鼠心肌组织CD11a、CD11b和CD11c的表达逐渐减弱。 RT-PCR显示,CD11a、CD11b、CD11c各组均呈阳性表达。其中CD11a在P5d和P40d间,P5d和 P19d间比较（P>0.05）差异无统计学意义,其他各组间比较差异均有统计
学意义;CD11b在E18d、P5d、P19d和P40d分别比较（P>0.05）差异无统计学意义,其他各组差异均有统计学意义;CD11c各组间差异有统计学意义（P<0.01）。结论 CD11a、CD11b和CD11c在大鼠心肌的发育过程中出现表达量的变化,不同结构的整合素分子在心脏发育过程表现出相似的
表达规律,它们可能对心肌细胞的发育起重要的调控作用。     

Nonsteroidal antiinflammatory agents inhibit upregulation of CD11b,CD11c,and CD35 in neutrophils stimulated by formyl-methionine-Leucine-phenylalanine

Nonsteroidal antiinflammatory drugs (NSAIDs) inhibit PMN aggregation, chemotaxis, degranulation, and superoxide anion production stimulated by synthetic formyl peptides. Many of these functions are dependent upon receptors for the complement components C3b and iC3b (CD35 and CD11b, respectively), or the adherence molecules CD11b and CD11c. Using flow cytometry and specific monoclonal antibodies, we studied the effects of the NSAID piroxicam and indomethacin on the upregulation of these cell surface proteins on PMNs stimulated with FMLP, C5a, or ionomycin. Incubation of PMNs at 37 °C increased the expression of all three of these surface proteins. A further increase was induced by stimulation with FMLP, C5a, or ionomycin. Both piroxicam and indomethacin inhibited FMLP-induced upregulation of CD11b, CD1 le, and CD35, but neither drug affected the upregulation of these surface molecules induced by C5a or ionomycin. Furthermore, piroxicam had no effect on 37°C-induced upregulation of any of the surface proteins, while indomethacin showed no effect on 37°C-induced CD11b upregulation but suppressed CD11c and CD35 upregulation. Inhibition of surface protein upregulation by FMLP was not due to inhibition of FMLP binding to PMNs. We conclude that piroxicam and indomethacin inhibit FMLP receptor-mediated upregulation of CD 11b, CD11c, and CD35 in PMNs, but have no effect on the upregulation of these molecules by ionomycin or C5a. These data suggest that piroxicam and indomethacin interfere with postreceptor signaling events specific to PMN stimulation by FMLP.Supported by DHHS grant 1-K11-HL02016 and a grant from Pfizer Pharmaceutical Company.     

Aberrant expression of CD7, CD56, and CD79a antigens in acute myeloid leukemias

The prognostic significance of selected markers of leukemic cells is well known. CD7 and CD56 expression at diagnosis has been associated with low remission rates and biological aggressiveness in a significant proportion of acute leukemias. Among 46 patients with acute myeloid leukemia, we found CD7 expression in 15 cases (32.6%) and CD56 positivity in 10 patients (21.7%). Six of these myeloid leukemia cases (13%) showed expression of both CD7 and CD56. Four of 46 (8.7%) patients expressed CD79a. Among the 10 that were acute myeloblastic leukemia, 8 expressed CD7, 4 expressed CD56, and 4 were positive for CD79a. Thus, these markers were expressed early in hemopoietic ontogeny in the lesser-differentiated acute myeloid leukemia subtypes, including FAB M0, M1, and M2. Whereas CD7 and CD56 were each positive in 4 cases of acute myelomonocytic leukemia (FAB M4 subtype), there was no CD79a expression in the M4 cases. CD7 is expressed by mature T cells, NK cells, and an immature myeloid cell subset. NK cells and a T cell subset express CD56. By contrast, CD79a is a B cell marker that is assigned a high score of 2.0 in the differentiation of acute leukemias of ambiguous lineage in the WHO classification. The aberrant expression of CD7, CD56, and CD79a, representing the capacity of these leukemias for trilineal expression of leukocyte differentiation antigens, portends a poor prognosis.     

CD317 is over-expressed in B-cell chronic lymphocytic leukemia,but not B-cell acute lymphoblastic leukemia

CD317 was first identified as a multiple myeloma-associated antigen. Here we report the expression of CD317 in normal B cells and B-cell malignancies. In normal bone marrow, CD317 demonstrates a biphasic expression pattern, with higher expression on stage 1 and stage 3 hematogones, but not on stage 2 hematogones. CD317 is over-expressed in B-cell chronic lymphocytic leukemia, and appears associated with negative CD38 expression. Moreover, CD317 is barely detectable in B-cell acute lymphoblastic leukemia. Our results suggest that CD317 expression might be of prognostic significance for B-CLL, and CD317 could be used as a new marker for minimal residual disease detection in B-ALL.     

伴11号染色体三体急性髓系白血病的细胞遗传学、免疫表型和临床特征分析

目的 分析伴有11号染色体三体(+11)的急性髓系白血病(AML)患者细胞遗传学、免疫表型和临床特征.方法 采用骨髓直接法和24小时短期培养法制备染色体标本,用G显带技术,对580例AML患者进行核型分析.用免疫荧光标记法及流式细胞术进行免疫表型检测,同时对其临床资料进行回顾性分析.结果 在580例成人AML中,伴有+11的患者10例,占1.7%,平均年龄65.5岁(45～78岁),其中8例患者超过60岁.核型分析提示4例合并伴有+8染色体,3例合并伴有del(5q),6例具有复杂核型.病例中原始细胞免疫表型分析显示原始细胞标记的CD34和(或)CD117始终表达.这些患者的完全缓解率为33.3%,中位存活时间仅80.5天.结论 伴+11的急性髓系白血病是一类异质性疾病,其患者核型复杂,白血病细胞具有原始细胞形态特点及早期原始细胞免疫标记特征,临床上表现为完全缓解率低和预后差.     

急性早幼粒细胞白血病中CD117和CD34共表达的临床意义

目的：研究CD117和CD34在成人急性非淋巴细胞自血病（Acute nonlymphoblastic leukemia，ANLL）M1～M2型和急性早幼粒细胞白血病（Acute promyelocytic leukemia，arE）M3患者中的表达，重点探讨M3患者CD117和CD34共表达（CD117／CD34共表达）的临床意义。方法：将研究病例分为M1～M2和M3二组，采用流式细胞术（Flow cytometery，FCM）随机检测54例M3和63例M1～M2二组初诊患者骨髓单个核细胞（BMMNC）髓系抗原CD117和干（祖）细胞抗原CD34的表达；比较M1～M2和M3二组ANLL患者中CD117、CD34表达的阳性率的差异，以及CD13、CD33和CD117分别与CD34共表达的阳性率差异。结果：CD117在M1～M2组患者中表达的阳性率是71．4／％（45／63），在M3组表达的阳性率为66．7％（36／54），差异无统计学意义（P=0．58）；CD34在M1～M2和M3二组中表达的阳性率分别为66．7％（42／63）和11．1％（6／54），差异有统计学意义（P=0．000）；二组ANLL的CD117／CD34共表达阳性率分别为71．1％（45／63）和7．4％（4／54），其差异有统计学意义（P=0．000）。结论：CD117可作为AL的髓系免疫学标志，但其在ANLL中的表达缺乏系列内阶段特异性。M3患者的CD34表达和CD117／CD34共表达的阳性率低于M1～M2者；CD117／CD34共表达可作为M1～M2和M3鉴别诊断的免疫学分型参考指标。     

Up-regulation of ICAM-1, CD11a/CD18 and CD11c/CD18 on human THP-1 monocytes stimulated by Streptococcus suis serotype 2

Streptococcus suis serotype 2 is known to be a major pathogen of swine, causing mainly meningitis. It is also a zoonotic agent leading predominantly to meningitis in humans working in close contact with pigs. In this study, we investigated the ability of S. suis to up-regulate the expression of adhesion molecules involved in inflammation, using an enzyme-linked immunosorbent assay. S. suis serotype 2 stimulated the up-regulation of the expression of intercellular adhesion molecule-1 (ICAM-1, CD54), CD11a/CD18 and CD11c/CD18 on human THP-1 monocytes, but did not change that of ICAM-1, vascular cell adhesion molecule-1 (VCAM-1, CD106) and E-selectin (CD62E) on human endothelial cells. The up-regulation of adhesion molecules was time- and bacterial concentration-dependent, and cell wall components were largely responsible for such stimulation. To a lesser extent, purified haemolysin of S. suis also stimulated adhesion molecule expression. Stimulation of monocytes with strains of different origin showed that there was no clear tendency for human strains to induce a higher expression of adhesion molecules than strains from diseased pigs. Finally, monocytes stimulated with S. suis also showed an increase in adherence to endothelial cells. Hence, S. suis is capable of up-regulating important adhesion molecules involved in inflammation, which may result in an increased leucocyte recruitment into sites of infection, thus providing a possible mechanism for some of the inflammatory features of meningitis caused by this pathogen.     

A CD44 monoclonal antibody differentially regulates CD11a/CD18 binding to intercellular adhesion molecules CD54, CD102 and CD50

We have made a monoclonal anti-CD44 antibody which is able to activate the leukocyte integrin CD11a/CD18. Activated T cells strongly aggregated, and the aggregation was shown to be intercellular adhesion molecule (ICAM)-1 (CD54) and ICAM-2 (CD102) dependent. Using purified ICAM coated on plastic, only binding to ICAM-1 was increased by the CD44 antibody, whereas activation by phorbol ester increased binding to both ICAM-1 and ICAM-3. The binding to ICAM-2 was not affected by either treatment. These findings show that the CD11a/CD18 integrin can be activated in a ligand-specific manner by engagement of CD44.