白细胞粘附分子单克隆抗体对成纤维细胞增殖作用的影响

目的探讨抗白细胞粘附分子即白细胞分化抗原（ＣＤ１１Ｂ，ＣＤ１８，ＣＤ５４）单克隆抗体对成纤维细胞的体外增殖作用的影响。方法采用３Ｈ胸腺嘧啶核苷掺入法（３ＨＴＤＲ）结合双抗夹心酶联免疫实验的方法，测定成纤维细胞的增殖和胶原分泌的水平。结果白细胞粘附分子的单克隆抗体ＣＤ１１Ｂ、ＣＤ１８、ＣＤ５４能抑制成纤维细胞（Ｌ９２９）的增殖，并且ＣＤ１１Ｂ与ＣＤ５４、ＣＤ１８与ＣＤ５４的单克隆抗体联合抑制作用更明显；其抑制作用分别为ＣＤ１１Ｂ、ＣＤ１８、ＣＤ５４单独使用的７．９、１．２５、２．１倍。并可减少成纤维细胞株（Ｌ９２９）胶原的分泌，抗体的协同作用分别为ＣＤ１１Ｂ、ＣＤ１８、ＣＤ５４的３、２．６、２．５倍。结论ＣＤ１１Ｂ、ＣＤ５４、ＣＤ１８的单克隆抗体可抑制成纤维细胞的增殖和胶原的分泌，可能在肺纤维化的治疗中具有潜在的应用价值。     

系统性红斑狼疮患者淋巴细胞粘附分子表达的观察

用流式细胞术及免疫双荧光染色法，分析了３５例系统性红斑狼疮（ＳＬＥ）患者外周血淋巴细胞粘附分子表型（ＣＤ＿（１１ａ）／ＬＦＡ－ｌα、ＣＤ＿（１８）／ＬＦＡ－１β、ＣＤ＿（５４）／ＩＣＡＭ－１）。结合淋巴细胞变化对ＳＬＥ作进一步探讨。结果发现ＳＬＥ活动期ＣＤ＿（１１ａ）、ＣＤ＿（１８）表达随ＣＤ＿４细胞减少而降低、ＣＤ＿８细胞增多而增高，ＣＤ＿（５４）在ＣＤ＿（２０）细胞上亦增高。此外，ＣＤ＿８细胞的ＣＤ＿（１８）增高与ＣＤ＿４ＣＤ＿（４５）ＲＡ￣＋细胞降低呈负相关（Ｐ＜０．０５），而与ＣＤ＿（２０）细胞的ＣＤ＿（５４）增高呈正相关（Ｐ＜０．０１）。提示粘附分子可能在ＳＬＥ发病机理中具有重要意义。     

合成多肽体外诱导乙肝病毒抗原特异性T杀伤细胞实验研究

目的及方法 为探讨ＨＢＶ抗原特异性细胞毒Ｔ细胞（ＨＢＶ－ＣＴＬ），根据ＨＢｃＡｇ的ＨＬＡ分子结合关键序列合成抗原多肽２段，分别与转铁蛋白（Ｔｆ），抗ＣＤ单克隆抗体（ＣＤ３ｍＡｂ）和ＩＬ－２联合体外诱导ＨＢＶ－ＣＴＬ，应用＾３Ｈ－ＴｄＲ释放法分别测定ＨＢＶ－ＣＴＬ对ＨＢＶＤＮＡ转染的ＨｅｐＧ２．２．１５细胞特异性活性及无ＨＢＶＤＮＡ转染的ＨｅＰＧ２细胞的非特异性杀伤率。结果 ＨＢＶ－ＣＴＬ对ＨＢＶＤ     

莲心碱对自发性高血压大鼠血管平滑肌细胞增殖及对PDGF—B,bFGF,c …

用［＾３Ｈ］胸腺嘧啶核苷（［＾３Ｈ］ＴｄＲ）掺入法、电镜、免疫组化和原位杂交方法，在自发性高血压大鼠（ＳＨＲ）观察了莲心碱（Ｌｉｌｅｎ）对血管平滑肌细胞（ＶＳＭＣ）增殖的作用及对生长因子ＰＤＧＦ－Ｂ、ｂＦＧＦ及其相关癌基因ｃ－ｓｉｓ和ｃ－ｍｙｃ表达的影响。结果发现Ｌｉｅｎ在降低ＳＨＲ血压同时，能减少ＶＳＭＣ的线粒体，粗面内质网和［＾３Ｈ］ＴｄＲ掺入量，并能逆转ＶＳＭＣ增殖对ＰＤＧＦ０Ｂ、ｂＦＧＦ抗     

CD+4自然杀伤T细胞在慢性乙型肝炎病毒感染中的作用

目的 了解ＣＤ４＾＋、ＣＤ８＾＋自然杀伤（ＮＫ）Ｔ细胞在慢性ＨＢＶ感染外周轿中的分布情况,并对其细胞毒性进行分析,阐明其在慢性ＨＢＶ感染中的作用。方法 常规分离外周上核细胞（ＰＢＭＣＳ）,用重组人白细胞介素－１２／２诱导１４ｄ,以鼠抗人ＣＤ４单克隆抗体或抗人ＣｍＡｂ与抗人ＣＤ５６ｍＡｂ分别标记细胞样品,流式细胞术（ＦＣＭ）分析,ＣＤ４＋ＣＤ５６＾＋同时阳性的细胞,即为ＣＤ４＾＋－ＮＫ－Ｔ细胞;Ｃ     

胃癌组织DCC基因（VNTR）的杂合性丢失和Bcl—2蛋白的表达

目的：为了研究ＤＣＣ基因的杂合性丢失（ＬＯＨ）和Ｂｃｌ－２蛋白过度表达在胃癌发生中的作用，方法：采用ＰＣＲ方法及免疫组织化学技术检测了胃癌组织ＤＣＣ基因的ＬＯＨ和Ｂｃｌ－２蛋白的表达。结果：结果发现，胃癌（信息个体）ＬＯＨ发生率为５４５％（１８／３３），Ｂｃｌ－２蛋白表达阳性率为６０％（３０／５０）；ⅢⅣ期胃癌ＬＯＨ发生率（８２２％，１５／１８）显著高于ⅠⅡ期胃癌２０％，３／１５）（Ｐ＜００１）；Ｂｃｌ－２蛋白的表达与ＤＣＣ基因的ＬＯＨ及胃癌大小、分化、淋巴结转移、浆膜浸润、临床分期及Ｌａｔｌｒｅｎ’ｓ分型无显著相关。结论：以上结果提示，ＤＣＣ基因的ＬＯＨ和Ｂｃｌ－２蛋白的高表达均参与了胃癌的发生，ＤＣＣ基因的ＬＯＨ是胃癌发生的晚期事件，其致癌机制与Ｂｃｌ－２有所不同     

细胞间粘附分子—1与脑缺血再灌注损伤

细胞间粘附分子－１是在血管内皮细胞表达的免疫球蛋白超家族成员之一。它可以作为配基与白细胞表面表达的ＬＦＡ－１（ＣＤ１１ａ／ＣＤ１８）和Ｍａｃ－１（ＣＤ１１ｂ／ＣＤ１８）分子相结合,介导白细胞与血管壁内细胞的粘附及白细胞穿出血管壁,从而在脑缺血及脑缺血再灌注损伤中起到重要作用。     

一组慢性淋巴增殖性疾病的实验室与临床特征

目的：进一步认识慢性淋巴增殖性疾病（ＣＬＤ）的临床及实验室特征。方法：从临床经过、形态学、免疫标记等方面分析该组病例。结果：Ｂ细胞慢性淋巴细胞白血病（Ｂ－ＣＬＬ）除具有成熟小淋巴细胞特征外，ＣＤ５＾＋和ＳｍＩｇ＾＋是其特殊的表型形式；毛细胞白血病（ＨＣＬ）以全血细胞减少和巨脾为特征，ＣＤ１１Ｃ、ＣＤ２５和超微结构对其诊断有极大帮助；本文尚对伴有绒毛淋巴细胞的脾淋巴瘤（ＳＬＶＬ）、Ｔ细胞幼稚淋巴细胞     

应用含CpG基序的寡核苷酸增强乙型肝炎病毒基因疫苗诱导的细胞免疫应答

目的 探讨人工合成的含ＣｐＧ基序的寡核苷酸（ＯＤＮ）作为佐剂对乙型肝炎病毒（ＨＢＶ）基因疫苗诱导小鼠产生细胞免疫应答的影响。方法 构建编码ＨＢＶ基因疫苗,人工合成含ＣｐＧ基序（ｍｏｔｉｆ）的硫代磷酸寡核苷酸作为佐剂,以Ｂａｌｂ／ｃ．１－Ｓ小鼠作为实验动物进行免疫接种;采用＾３Ｈ－ＴｄＲ法、＾５１Ｃｒ４ｈ释放法等分别检测免疫小鼠的淋巴细胞增殖和杀伤功能。结果 与空载体对照组相比较,ＨＢＶ基因疫苗诱发     

普伐他汀对氧化修饰低密度脂蛋白诱导的人外周血单核细胞 …

目的：探讨普伐他汀对氧化修饰低密度脂蛋白（ｏｘＬＤＬ）诱导的人外周血单核细胞（ＰＢＭｓ）增殖、粘附和分泌功能的影响及其除调脂外的抗动脉粥样硬化（ＡＳ）作用。方法在体外分离培养人ＰＢＭｓ,经ｏｘＬＤＬ诱导后,观察不同浓度普伐他汀对其增殖,粘附分子ＣＤ１１ｂ水平及对人脐静脉内皮细胞（ＨＵＶＥＣ）的粘附和分泌ＴＮＦ－α、ＩＬ－８的影响。结果普伐他汀呈浓度依赖方式抑制ｏｘＬＤＬ诱导的ＰＢＭｓ增殖、粘附和分     

High-density lipoproteins inhibit fibrinogen binding on adenosine diphosphate-activated monocytes.

High levels of fibrinogen and low levels of high-density lipoprotein (HDL) cholesterol were reported to be risk factors for coronary heart disease. CD11b/CD18, a fibrinogen-binding protein, is expressed on the surface of monocytes, which play a crucial role in the formation of atherosclerotic lesions. In the present study, we investigate the effects of antibodies against CD11b and CD18, as well as HDL3 and low-density lipoprotein (LDL) cholesterol on fibrinogen binding on monocytes. We find that binding of fibrinogen on monocytes activated with adenosine diphosphate (ADP) was reduced to 66.0+/-8.3% (mean +/- SD) in the presence of anti-CD11b antibodies (12.5 microg/ml; P < or = 0.02) and to 54.5+/-4.9% in the presence of anti-CD18 antibodies (20 microg/ml; P < or = 0.01), respectively. Fibrinogen binding on Cytochalasin-B-activated monocytes was reduced to 79.8+/-6.0% in the presence of anti-CD18 (20 microg/ml; P < or = 0.05). Incubation of ADP-activated monocytes with HDL3 (0.5 g/l) led to a lowering of fibrinogen binding to 65.0+/-6.6% (P < or = 0.05). No effect of HDL3 on fibrinogen binding was seen on Cytochalasin-B-activated monocytes. A slight, non-significant stimulatory effect of LDL on fibrinogen binding on ADP-activated but not on Cytochalasin-B-activated monocytes was additionally observed. Neither incubation with HDL3 or with LDL had a significant influence on ADP-activated cellular binding of anti-CD11b or anti-CD18 antibodies. The inhibition of fibrinogen binding on monocytes in the presence of HDL3 is a major new finding of this study. Since inhibition of fibrinogen binding in the presence of HDL might impair both monocyte recruitment to the arterial wall and foam cells formation, our findings suggests a novel mechanism by which HDL may prevent development of arteriosclerosis.     

转化生长因子β1单克隆抗体干预成纤维细胞增殖的体外研究

目的观察抗转化生长因子β１（ＴＧＦβ１）单克隆抗体对成纤维细胞（ＦＢ）增殖及胶原合成的影响。方法将肺泡巨噬细胞（ＡＭ）培养上清液与Ｌ９２９成纤维细胞株共同孵育,并加入不同剂量ＴＧＦβ１单克隆抗体,用３Ｈ胸腺嘧啶掺入法观察ＦＢ增殖及胶原合成的情况。结果抗ＴＧＦβ１单克隆抗体能够抑制ＡＭ条件上清液引起的ＦＢ增殖,在一定剂量范围内（１０μｇ／ｍｌ）呈剂量效应关系。抑制作用在１０μｇ／ｍｌ时达到最大并使ＦＢ培养上清Ⅳ型胶原的合成减少３２％。结论提示抗ＴＧＦβ１单克隆抗体的应用可能为肺纤维化的治疗提供潜在的新途径。     

CD9 participates in endothelial cell migration during in vitro wound repair

CD9, a widely expressed membrane protein of the tetraspanin family, has been implicated in diverse functions, such as signal transduction, cell adhesion, and cell motility. We tested the effects of an anti-CD9 monoclonal antibody (ALMA.1) on the migration and proliferation of human vascular endothelial cells (ECs) during repair of an in vitro mechanical wound mimicking angiogenic processes. ALMA.1 induced dose-dependent inhibition of wound repair with a 35+/-1.5% decrease at 20 microg/mL. Only cell migration was affected, because the rate of proliferation of ECs at the lesion margin was not modified and because the inhibition of repair was also observed for nonproliferating irradiated ECs. Monoclonal antibodies against CD63 tetraspanin (H5C6) and control mouse IgG (MOPC-21) were inactive. CD9, one of the most abundant proteins at the surface of ECs, colocalized with beta(1) or beta(3) integrins on EC membranes in double-labeling immunofluorescence experiments with ALMA.1 and an anti-beta(1) (4B4) or anti-beta(3) (SDF.3) monoclonal antibody. Moreover, ALMA.1 and 4B4 had additive inhibitory effects on lesion repair, whereas 4B4 alone also inhibited EC proliferation. In transmembrane Boyden-type assays, ALMA.1 induced dose-dependent inhibition of EC migration toward fibronectin and vitronectin with 45+/-6% and 31+/-10% inhibition, respectively, at 100 microg/mL. 4B4 inhibited migration toward fibronectin at 10 microg/mL but had no effect in the case of vitronectin. Adhesion of ECs to immobilized anti-CD9 monoclonal antibodies induced tyrosine-phosphorylated protein levels similar to those observed during interactions with beta(1) or beta(3) integrins. These results point to the involvement of CD9 in EC adhesion and migration during lesion repair and angiogenesis, probably through cooperation with integrins. As such, CD9 is a potential target to inhibit angiogenesis in metastatic and atherosclerotic processes.     

结缔组织生长因子及其抗体对人胃成纤维细胞生物学功能的影响

目的 研究结缔组织生长因子(CTGF)及其抗体对人胃成纤维细胞增殖、移行、合成细胞外基质(ECM)的影响.方法 (1)应用四唑盐(MTT)比色法检测不同浓度的CTGF(5、20、50、100 ng/ml)及其抗体(0.1、0.5、1 μg/ml)对人胃成纤维细胞增殖的影响.(2)应用羟脯氨酸法检测不同浓度的CTGF及其抗体对人胃成纤维细胞分泌胶原蛋白的影响.(3)应用Transwell小室法检测不同浓度的CTGF及其抗体对人胃成纤维细胞迁移能力的影响.结果 5 ～ 10 ng/ml CTGF可剂量依赖性地促进入胃成纤维细胞增殖;20～ 100 ng/ml CTGF可剂量依赖性地促进人胃成纤维细胞分泌胶原蛋白;20～ 100 ng/ml CTGF可剂量依赖性地促进人胃成纤维细胞迁移.另一方面,0.1～1μg/ml CTGF抗体可剂量依赖性地抑制人胃成纤维细胞增殖;0.5、1 μg/ml CTGF抗体可剂量依赖性地抑制人胃成纤维细胞分泌胶原蛋白;0.5、1 μg/ml ETGF抗体可剂量依赖性地抑制人胃成纤维细胞迁移.以上各实验组与相应对照组比较均有显著性差异(P＜0.05).结论 一定浓度范围内的CTGF能剂量依赖性地促进人胃成纤维细胞增殖、分泌胶原蛋白及迁移,这表明CTGF参与了胃硬癌间质纤维化进程,在间质纤维化进程的各环节发挥重要作用.而一定浓度范围内的CTGF抗体可剂量依赖性地抑制这些效应,这为胃硬癌的临床治疗提供了新的思路.     

Inhibition of human B-cell lymphoma growth by CD40 stimulation

CD40 is a molecule present on B lymphocyte lineage cells that is important in B-cell differentiation and activation. Signaling through CD40 has been shown to exert costimulatory signals on normal B cells resulting in proliferative and differentiation responses. Examination of several B-cell lymphomas showed cell-surface expression of the CD40 molecule. Incubation of these lymphomas with anti-CD40 antibodies resulted in significant growth inhibition in vitro. Cross-linking of the CD40 antibodies resulted in even greater inhibition of proliferation. A recombinant soluble human CD40 ligand was also shown to inhibit lymphoma proliferation. When various human B-cell lymphomas were transferred into mice with severe combined immune deficiency, the treatment of the mice with anti-CD40 antibodies resulted in significant increases in survival showing that anti-CD40 is efficacious after in vivo administration. Thus, CD40 stimulation by either the antibody or soluble ligand directly inhibits human B-cell lymphoma growth and therefore, may be of significant clinical use in their treatment.     

Pirfenidone inhibits the proliferation of fibroblasts from patients with active Crohn’s disease

Objective: One-third of Crohn’s disease (CD) patients develop intestinal strictures that require repeated surgical intervention. Current anti-inflammatory therapies have limited effect on stricture development, which necessitates the exploration of new pharmacological approaches. Pirfenidone (PFD), a novel anti-fibrotic agent, was recently approved in Europe for the treatment of idiopathic pulmonary fibrosis (IPF). We hypothesized that observations in IPF could be transferable to intestinal fibrosis and that PFD inhibits the proliferation and extracellular matrix (ECM) turnover of gut-derived fibroblasts from CD patients.

Material and methods: Fibroblasts were isolated from biopsies of inflamed (n?=?8) and non-inflamed (n?=?5) colonic mucosa. Expression of CD90 and alpha-smooth muscle actin (αSMA) expression was determined by flow cytometry. The fibroblasts were cultured with PFD (0.5, 1.0 and 2.0?mg/ml). Proliferation was evaluated with CellTiter 96^® AQ_ueous One Solution Cell Proliferation Assay. Production of matrix metalloproteinase-3 (MMP-3), tissue inhibitor of metalloproteinases-1 (TIMP-1) and collagen were assessed using ELISA and calorimetric assays, respectively.

Results: The majority of the fibroblasts were αSMA-positive myofibroblasts. PFD inhibited fibroblast proliferation [0.94 (PFD 0.5?mg/ml); 0.76 (1.0?mg/ml); 0.58 (2.0?mg/ml)] and production of MMP-3 [0.85 (0.5?mg/ml); 0.74 (1.0?mg/ml); 0.63 (2.0?mg/ml)] dose-dependently (both p?=?0.0001). The anti-proliferative effect of PFD was reversible (p?=?0.0001), indicating that PFD does not act by an irreversible cytotoxic mechanism. PFD did not influence neither TIMP-1 nor collagen production.

Conclusion: PFD inhibited the proliferation and the production of MMP-3 dose-dependently in gut-derived fibroblast from CD patients. Our observations support further studies on PFD in stricturing CD.     

Relaxin modulates cardiac fibroblast proliferation, differentiation, and collagen production and reverses cardiac fibrosis in vivo

Cardiac fibrosis is a key component of heart disease and involves the proliferation and differentiation of matrix-producing fibroblasts. The effects of an antifibrotic peptide hormone, relaxin, in inhibiting this process were investigated. We used rat atrial and ventricular fibroblasts, which respond to profibrotic stimuli and express the relaxin receptor (LGR7), in addition to two in vivo models of cardiac fibrosis. Cardiac fibroblasts, when plated at low density or stimulated with TGF-beta or angiotensin II (Ang II), accelerated fibroblast differentiation into myofibroblasts, as demonstrated by significantly increased alpha-smooth muscle actin expression, collagen synthesis, and collagen deposition (by up to 95% with TGF-beta and 40% with Ang II; all P < 0.05). Fibroblast proliferation was significantly increased by 10(-8) m and 10(-7) m Ang II (63-75%; P < 0.01) or 0.1-1 microg/ml IGF-I (27-40%; P < 0.05). Relaxin alone had no marked effect on these parameters, but it significantly inhibited Ang II- and IGF-I-mediated fibroblast proliferation (by 15-50%) and Ang II- and TGF-beta-mediated fibroblast differentiation, as detected by decreased expression of alpha-smooth muscle actin (by 65-88%) and collagen (by 60-80%). Relaxin also increased matrix metalloproteinase-2 expression in the presence of TGF-beta (P < 0.01) and Ang II (P < 0.05). Furthermore, relaxin decreased collagen overexpression when administered to two models of established fibrotic cardiomyopathy, one due to relaxin deficiency (by 40%; P < 0.05) and the other to cardiac-restricted overexpression of beta2-adrenergic receptors (by 58%; P < 0.01). These coherent findings indicate that relaxin regulates fibroblast proliferation, differentiation, and collagen deposition and may have therapeutic potential in diseased states characterized by cardiac fibrosis.     

转化生长因子—β1单克隆抗体对大鼠肺纤维化的治疗观察

目的探讨转化生长因子－β（ＴＧＦ－β）单克隆抗体对博莱霉素所致肺间质纤维化的作用。方法结合体内和体外实验，利用３Ｈ－胸腺嘧啶核苷（３Ｈ－ＴｄＲ）掺入法和Ｎｏｒｔｈｅｒｎ杂交法。结果表明大鼠肺纤维化模型中肺泡巨噬细胞的条件培养基能促进成纤维细胞的增殖和胶原ｍＲＮＡ的表达。ＴＧＦ－β１单克隆抗体对其有抑制作用，同时亦能减轻肺组织的病变程度和胶原ｍＲＮＡ的表达。结论ＴＧＦ－β１单克隆抗体可部分地抑制成纤维细胞增殖和胶原合成。     

Anti-Fas-induced apoptosis in chondrocytes reduced by hyaluronan: evidence for CD44 and CD54 (intercellular adhesion molecule 1) invovement

OBJECTIVE: To investigate the in vitro effect of therapeutic hyaluronan (HA) of 500-730 kd on anti-Fas-induced apoptosis of chondrocytes from osteoarthritis (OA) patients, and to assess its mechanism of action by analyzing the role of the 2 HA receptors, CD44 and CD54 (intercellular adhesion molecule 1 [ICAM-1]). METHODS: Chondrocytes isolated from human OA knee cartilage were cultured and the effect of HA on both spontaneous and anti-Fas-induced apoptosis was evaluated. Apoptosis was analyzed by JAM test (for quantitative analysis of fragmented DNA), cell death detection immunoassay (for quantitative analysis of oligonucleosome), TUNEL assay, and electron microscopy. Blocking experiments with anti-CD44 and anti-CD54 alone or in combination were performed to investigate the HA mechanism of action. RESULTS: Both quantitative tests demonstrated that anti-Fas significantly induced apoptosis of isolated OA chondrocytes. HA at 1,000 microg/ml significantly reduced the anti-Fas-induced apoptosis of chondrocytes but did not affect spontaneous chondrocyte apoptosis. These data were also confirmed by TUNEL staining and by electron microscopy morphologic evaluation. The antiapoptotic effects of HA on anti-FAS-induced chondrocyte apoptosis were significantly decreased by both anti-CD44 (mean +/- SD 57 +/- 12% inhibition) and anti-ICAM-1 (31 +/- 22% inhibition). The mixture of the 2 antibodies had an additive effect, since the rate of inhibition increased to 87 +/- 13%. CONCLUSION: These data demonstrate that 500-730-kd HA exerts an antiapoptotic effect on anti-FAS-induced chondrocyte apoptosis by binding its specific receptors (CD44 and ICAM-1). Furthermore, this HA fraction may be able to slow down chondrocyte apoptosis in OA by regulating the processes of cartilage matrix degradation.     

Increased production of hydrogen peroxide and expression of CD11b/CD18 on alveolar macrophages in patients with active pulmonary tuberculosis

Setting: Alveolar macrophages (AM) are important in host defense against Mycobacterium tuberculosis (TB). β2-integrin, especially CD11a/CD18 and CD11b/CD18, are implicated in leukocyte migration, antigen presentation, phagocytosis, and production of reactive oxygen speciesObjective: To explore the functional relevance of β2-integrin expression to intracellular H₂O₂ capacity of AM in TB patients.Design: In a prospective study, AM retrieved from 18 active pulmonary TB patients and 18 normal subjects were assessed for β2-integrin expression and intracellular H₂O₂ metabolism capacity by loading with anti-CD11a/CD18, anti-CD11b/CD18 monoclonal antibodies and 2′,7′ dichlorofluorescein diacetate (DCFH-DA) respectively, and analyzed by flow cytometry. AM from 8 normal subjects were stimulated with tumor necrosis factor-alpha (TNF-α, 10⁵ units/ml) to examine the relationship between H₂O₂ production and CD11b/CD18 expression.Results: The magnitude of DCFH oxidation and CD11b/CD18 expression of AM was higher in TB patients than in normal subjects. The CD11b/CD18 expression was related to the magnitude of DCFH oxidation, but not to lymphocyte numbers or subpopulations (CD4, CD8, CD25). Stimulation of AM with TNF-α increased H₂O₂ production and CD11b/CD18 expression. Pretreatment with CD11b/CD18 monoclonal antibodies inhibited TNF-α-induced H₂O₂.Conclusion: AM in TB patients possessed a higher capacity of oxidant metabolism. The increased CD11b/CD18 expression may be related to the increased respiratory burst response in AM against mycobacterial invasion.