类风湿关节炎患者红细胞C3b受体数目发迹及基因多态性分析

目的 分析类风湿关节炎（ＲＡ）患者Ｃ３ｂ受体（Ｃ３ｂＲ）表达数目及Ｃ３ｂＲ基因多态性分布规律，探讨Ｃ３ｂＲ数目改变的可能原因。方法 分别测定６３例ＲＡ患者及健康献血员６０人的红细胞Ｃ３ｂ受体花环率（Ｃ３ｂＲＲ）及免疫复合物花环率（Ｃ３ｂＩＣＲ）。用限制性片段长度多态（ＲＦＬＰ）分析及Ｓｏｕｔｈｅｒｎ ｂｌｏｔｔｉｎｇ杂交技术检测Ｃ３ｂＲ基因多态性。结果 ＲＡ患者红细胞Ｃ３ｂ－ＲＲ和Ｃ３ｂ－ＩＣＲ分     

雷公藤多甙对类风湿性关节炎患者红细胞免疫功能的影响

雷公藤多甙对类风湿性关节炎患者红细胞免疫功能的影响日照市人民医院（２７６８００）刘加军青岛医学院附属医院王伟，王颜刚我们用雷公藤多贰治疗类风湿性关节炎（ＲＡ）２６例，并测定其治疗前后红细胞Ｃ３ｂ受体（Ｃ３ｂＲ）花环率及红细胞免疫复合物（ＩＣ）花环率。...     

不同病期的老年类风湿性关节炎患者红细胞免疫功能的变化

观察不同病期老年类风湿性关节炎患者红细胞功能的动态变化、并以此作为判断疗效、观察病情变化的指标。对２５例老年类风湿性关节炎患者活动期与缓解期的红细胞Ｃ３ｂ受体（Ｃ３ｂＲ）花环率及红细胞免疫复合物（ＩＣ）花环率进行了检测，结果活动期红细胞免疫免疫功能显著低于对照组；而缓解期则有所恢复，其Ｃ３ｂＲ花环率均低于正常组。     

冠心病患者红细胞免疫功能的变化

本文测定了正常人及冠心病患者的红细胞免疫功能。结果表明，冠心病患者的红细胞Ｃ３ｂ受体花环率（ＲＢＣ－Ｃ３ｂＲＲ）降低，红细胞免疫复合物花环率（ＲＢＣ－ＩＣＲ）及循环免疫复合物（ＣＩＣ）增高；且ＣＩＣ与ＲＢＣ－Ｃ３ｂＲＲ呈负相关，与ＲＢＣ－ＩＣＲ呈正相关；ＲＢＣ－Ｃ３ｂＲＲ与ＲＢＣ－ＩＣＲ呈负相关，提示冠心病患者存在红细胞免疫功能低下，可能为继发性改变。     

风湿性心脏病患者红细胞免疫功能的初步探讨

应用红细胞Ｃ３ｂ（ＲＢＣ－Ｃ３ｂ）受体花环试验及红细胞免疫复合物（ＲＢＣ－ＩＣ）花环试验，对６０例风湿性心脏病（简称风心病）患者及７１例正常人的红细胞免疫功能进行了对照研究。结果表明，风心病患者ＲＢＣ－Ｃ３ｂ受体花环率明显低于正常人（Ｐ＜０．０１），ＲＢＣ－ＩＣ花环率明显高于正常人（Ｐ＜０．００１），提示风心病发病与红细胞免疫功能异常有密切关系。风心病患者ＲＢＣ－Ｃ３ｂ受体花环率及ＲＢＣ－ＩＣ花环率与瓣膜损害的数量，无明显关系（Ｐ＞０．０５）。ＲＢＣ－ＩＣ花环率在中至重度心力衰竭组明显高于心功能正常及轻度心力衰竭组（Ｐ＜０．００１），ＲＢＣ－Ｃ３ｂ受体花环率两组无明显差异（Ｐ＞０．０５）。     

Ⅱ型糖尿病患者红细胞免疫功能、SOD含量的变化及其意义

Ⅱ型糖尿病患者红细胞免疫功能、ＳＯＤ含量的变化及其意义日照市人民医院（２７６８００）吕祖英刘加军我们对２５例Ⅱ型糖尿病患者的红细胞Ｃ３ｂ受体（Ｃ３ｂＲ）花环率、红细胞循环免疫复合物（ＩＣ）花环率及红细胞超氧化物歧化酶（ＳＯＤ）含量进行了联合检测，现将...     

肺结核患者T淋巴细胞亚群,红细胞免疫功能与核仁组成区 …

目的 探讨结核病患者Ｔ淋巴细胞亚群，红细胞免疫功能及核仁组成相关嗜银蛋白（ＡｇＮＯＲｓ）的关系及其临床意义。方法 采用碱性磷酸酶抗碱性磷酸酶（ＡＰＡＡＰ）法，红细胞花环试验以及ＡｇＮＯＲｓ测定方法，对５９例肺结核患者和５０名正常对照组分别测定了外周血Ｔ淋巴细胞亚群，红细胞免疫Ｃ３ｂ受体花环率（Ｅ－Ｃ３ｂＲＲ）与红细胞循环免疫复合物花环率（Ｅ－ＩＣＲ），ＡｇＮＯＲｓ面积（ＧＡ），核面积（ＮＡ）及ＧＡ     

过敏性紫癜患者红细胞免疫功能与NK细胞活性的变化

目的 探讨红细胞免疫及天然杀伤细胞（ＮＫＣ）在过敏性紫癜（ＨＳＰ）发病中的可能作用。方法 红细胞免疫采用郭峰法测定２２例ＨＳＰ患者,红细胞Ｃ３ｂ受体花环率（ＲＢＣ－Ｃ３ｂＲＲ）,与免疫复合物受体花环率（ＲＢＣ－ＩＣＲ）,流式细胞仪与单克隆抗体（ＣＤ１６）测定ＮＫ细胞的活性。并与２０名正常体检儿童对照。结果 ＨＳＰ患者ＲＢＣ－Ｃ３ｂＲＲ及ＮＫＣ活性低于正常对照组（Ｐ〈０．０１）,ＲＢＣ－ＩＣＲ高于正     

消化系统易癌变疾病与癌症患者红细胞免疫功能变化及临床意义

消化系统易癌变疾病与癌症患者红细胞免疫功能变化及临床意义山东医科大学第二附属医院（２５００３３）林森蒋卫东山东医科大学附属医院赵宪时庆我们检测了部分消化系统易癌变疾病及癌症患者的红细胞Ｃ３ｂ受体花环率（ＲＣＲ）与免疫复合物花环率（ＲＩＣＲ），以探讨...     

补硒对大骨节病病区居民红细胞免疫功能的影响

给大骨节病病区１３￣１５岁居民每日口服亚硒酸钠硒２００ｕｇ，１２周后测定红细胞硒含量和谷胱甘肽过氧化物酶（ＧＳＨ－ｐｘ）活性，红细胞免疫粘附（ＲＣＩＡ）功能，血清ＲＣＩＡ调节功能和循环免疫复合物（ＣＩＣ）含量，以探讨补硒对病区居民ＲＣＩＡ功能的影响。病区居民补硒后红细胞硒含量，ＧＳＨ－ｐｘ活性和红细胞Ｃ３ｂ受体（ＲＢＣ－Ｃ３ｂＲ）花环率明显提高，血清ＲＣＩＡ花环抑制率明显降低，但补硒对红细胞免疫复     

Low number of complement C3b/C4b receptors (CR1) on erythrocytes from patients with essential mixed cryoglobulinemia, systemic lupus erythematosus and rheumatoid arthritis: relationship with disease activity, anticardiolipin antibodies, complement activation and therapy.

Our aim was to assess whether the amount of complement C3b/C4b receptors (CR1) on erythrocytes shows a correlation to disease activity in various connective tissue diseases such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA) and essential mixed cryoglobulinemia (EMC). Using an anti-CR1 monoclonal antibody, 26 patients with SLE, 34 with RA and 22 patients with EMC were investigated for erythrocyte CR1 expression. The control group consisted of 30 healthy individuals. The mean number of CR1/erythrocyte in the control group was 568 +/- 197 (range 174-1060), significantly higher than studied (EMC:379 +/- 248; p = 0.0005;SLE 147 +/- 56, p less than 0.0001; RA 298 +/- 177, p less than 0.0001). In patients with RA and in SLE, but not in patients with EMC, the number of CR1 numbers and anticardiolipin antibody (aCl) titers (r2 = 0.493; p = 0.034). A statistically significant correlation between CR1 numbers and CH50 values was found in patients with SLE, while in 3 patients with RA 4 months of therapy with cyclosporine A led to a further 30% reduction in CR1 number. Our conclusions are that (a) the decreased expression of erythrocyte CR1 is apparently a common feature of patients with various connective tissue diseases; (b) several acquired factors such as disease activity, complement activation, aCl and drugs may contribute to the loss of CR1 from erythrocytes; (c) in patients with RA and SLE, but not in patients with EMC, CR1 enumeration on erythrocytes may serve as a variable for clinical monitoring.     

Genetic polymorphism H131R of Fcγ receptor type IIA (FcγRIIA) in a healthy Finnish population and in patients with or without platelet-associated IgG

Abstract: Patients (n = 113) with histories of thrombocytopenia and with different profiles for platelet-associated IgG (PA-IgG) were subdivided according to the genetic polymorphism H131R in the Fcγ receptor type IIA (FcγRIIA). PA-IgG was measured by the direct platelet immunofluorescence test (PIFT), and GP IIbIIIa and/or GP Ib-specific PA-IgG was investigated by a modified version of the direct monoclonal antibody-specific immobilization of platelet antigens (MAIPA) assay. As a control, the distribution of FcγRIIA polymorphism H131R was determined among 93 healthy Finnish blood donors. The frequencies for H131 and R131 were 0.56 and 0.44 (CI: 0.37–0.51), respectively, which did not differ significantly from those in other Caucasian populations. The distribution of the genotypes HH131, HR131 and RR131 in the patients and controls did not differ significantly. In the HH131 group, the PA-IgG was higher than in the RR131 group (p = 0.082). Female patients with the genotype RR131 seemed to be younger than those with HH131 (p = 0.065). Among the female patients, a significantly greater number were under 40 yr old in the RR131 group than in the HH131 group (p = 0.0060). Within the RR131 group, the female patients were far younger than the male patients (median 29 vs. 61 yr; p = 0.0021). The results point to the heterogeneity of immune thrombocytopenia, which may partly explain the poor predictive value of PA-IgG studies.     

Genetic analysis of CR1 (the C3b complement receptor, CD35) expression on erythrocytes of HIV-infected individuals

The number of C3b receptor (CR1) molecules on erythrocytes is genetically determined by two codominant autosomal alleles. The genetic polymorphism of CR1 expression correlates with a Hind III restriction fragment length polymorphism (RFLP) of the CR1 gene. The relative frequency of individuals homozygous for the allele coding for low CR1 numbers is approximately 5% of the normal population. CR1 numbers/erythrocytes are significantly decreased in symptomatic HIV-infected individuals. Decreased CR1 expression correlates with the severity of disease. The present study investigated the CR1 genomic Hind III RFLP-related polymorphism in 79 HIV-infected individuals and 84 healthy subjects. Allele frequencies were found to be similar in both populations. Thus, there is no susceptibility nor resistance to HIV-infected linked to the CR1 gene. Defective expression of CR1 in HIV-infected patients is acquired through central and/or peripheral mechanisms.     

Association between urokinase gene 3'-UTR T/C polymorphism and Chinese patients with rheumatoid arthritis in Taiwan

OBJECTIVES: The purpose of this study was to investigate whether the urokinase gene 3'-UTR C/T polymorphism is a marker of susceptibility to or severity of rheumatoid arthritis (RA) in Chinese patients. METHODS: A total of 145 RA patients and 134 healthy control subjects were enrolled in this study. We identified the C/T polymorphism of the urokinase gene, which is mapped on the 3'-untranslated region (3'-UTR) on chromosome 10 by polymerase chain reaction (PCR). RESULTS: There were significant differences in the distribution of the urokinase gene 3'-UTR C/T polymorphism frequency between RA patients and subjects in the control group. However, we did not detect an, association between the urokinase gene 3'-UTR C/T polymorphism and rheumatoid factor (RF), extraarticular involvement or bone erosion in RA patients. CONCLUSION: The urokinase gene 3'-UTR "T" allele was associated with RA in Chinese patients in Taiwan.     

Defective reticuloendothelial system C3b mediated clearance in rheumatoid arthritis and vasculitis

C3b receptor mediated clearance by the reticuloendothelial system (RES) was tested in vivo using autologous C3b coated, technetium labelled erythrocytes in patients with rheumatoid arthritis (RA) and rheumatoid vasculitis. Diminished C3b mediated erythrocyte clearance was found in all patients with rheumatoid vasculitis and some patients with active RA. Normal C3b mediated clearance was found in some patients with previous vasculitis, in remission when tested. These results are consistent with the hypothesis that acquired dysfunction of RES C3b receptors is implicated in the pathogenesis of rheumatoid vasculitis.     

陷阱因子3在类风湿关节炎患者血清及外周血单核细胞中的表达研究

目的 研究类风湿关节炎(RA)患者血清及外周血单核细胞中DcR3的表达情况.方法 选取已确诊的60例类风湿因子(RF)(+)的RA患者并按照DAS28评分将其分为RAa组和RAb组,以30名体检健康者作为对照,酶联免疫吸附试验( ELISA)法检测各组血清可溶性陷阱因子3(DcR3)的表达情况.同时荧光实时定量聚合酶链反应(PCR)检测各组外周血单核细胞中DcR3的表达情况.采用t检验和X2检验进行统计学分析.结果 DcR3血清表达水平在DAS28＞2.6的RAb组为(264+72) ng/ml较健康对照组为(48±39) ng/ml明显升高(r=0.251,P＜0.05).而在DAS28＜2.6的RAa组则没有差异.DcR3基因的扩增倍数在RAb组为23.5±5.4,健康对照组为8.3±3.6,差异具有统计学意义(r=0.336,P＜0.05).结论 DcR3在RA患者血清及外周血单核细胞中表达增高,而其血清表达水平在风湿活动较高的患者则更加明显.     

侵袭性真菌感染患者细胞色素P_(450)2C19遗传多态性分析

目的 探讨细胞色素P_(450)2C19(CYP2C19)遗传多态性在侵袭性真菌感染患者中的分布情况.方法 采用PCR-限制性片段长度多态性(PCR-RFLP)技术检测134例侵袭性真菌感染患者和134例健康对照者CYP2C19基因2个主要单核苷酸多态性位点CYP2C19*2和CYP2C19*3的基因型,比较两组各等位基因频率及代谢型的比例.结果 侵袭性真菌感染病例组CYP2C19*1等位基因频率为58.2%,CYP2C19*2等位基因频率为36.6%,CYP2C19*3 等位基因频率为5.2%.对照组CYP2C19*1等位基因频率为63.4%,CYP2C19*2 等位基因频率为34.3%,CYP2C19*3 等位基因频率为2.2%,两组间差异无统计学意义.侵袭性真菌感染组纯合快代谢、杂合快代谢以及慢代谢型比例分别为33.6%、50.0%、16.4%,对照组比例为40.3%、48.5%、11.2%,两组差异无统计学意义.结论 在本组侵袭性真菌感染患者以及健康人群中存在明显CYP2C19遗传多态性,且近2/3患者为杂合快代谢型或慢代谢型.因此,在治疗过程中应重视CYP2C19遗传多态性对药物代谢的影响.     

Association of the nitric oxide synthase (eNOS) gene polymorphism with increased risk for both lupus glomerulonephritis and rheumatoid arthritis in a single genetically homogeneous population

Nitric oxide (NO), a short-lived gaseous free radical, synthesized from L-arginine by NO synthases (NOS), is a potent mediator of biologic responses involved in the pathogenesis of autoimmune rheumatic diseases, such as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). Most biological necessary NO is produced by the family of three NOS. To date, several functionally relevant genetic polymorphisms in the eNOS gene have been associated with various vascular, infectious and autoimmune diseases. To our knowledge, no study has explored these polymorphisms for both SLE and RA in the same population. The objective of this study was to investigate the influence of the eNOS gene intron 4 a/b VNTR polymorphism (a 27-base-pair tandem repeat-based polymorphism) on susceptibility to SLE and RA in patients living in the island of Crete, a genetically homogeneous population. A group of 145 healthy subjects and 190 SLE patients were included in this study. Similarly, a second group of 235 healthy controls and 202 RA patients were analysed. In both cases, patients and controls were sex- and age-matched. Herein we report that the presence of a/b genotype of the eNOS gene may act as a risk factor not for the presence of SLE but for the development of glomerulonephritis (OR 2.71, 95% CI: 1.4-5.2), while it may be a susceptibility gene for RA (OR: 2.005, 95% CI: 1.31-3.07). Thus, in our population, the a/b genotype of the eNOS gene represents a severity rather than a susceptibility genotype for SLE.     

Cytokine (IL-6) and chemokine (IL-8) gene polymorphisms among rheumatoid arthritis patients in Taiwan

OBJECTIVE:The involvement of cytokines and chemokines in the pathogenesis of rheumatoid arthritis (RA) is well studied; however, the genetic bases behind this is not well understood. The aim of this study was to examine whether -572 G/C polymorphism in the IL-6 gene and 2767 A/G polymorphism in the 3'-untranslated region (UTR) of the IL-8 gene are associated with rheumatoid arthritis (RA).METHODS:We enrolled 199 RA patients and 130 normal controls. Polymerase chain reaction was used to identify the IL-6 -572G/C and IL-8 3'-UTR 2767A/G polymorphisms. The relationships between clinical manifestations of RA and the polymorphisms of each gene were investigated by comparing the genotypes among RA patients with different clinical variables. RESULTS:We found no significant difference in the genotypic and allelic frequencies of the single nucleotide polymorphisms of IL-6 and IL-8 genes between RA patients and controls. Clinical characteristics such as age at onset, rheumatoid factor positivity, joint erosion and extra-articular manifestations were compared among patients with different genotypes of the IL-6 and IL-8 genes. We found that patients with IL-8 3'-UTR 2767AA genotype had a significantly younger age of onset of RA than patients without that genotype.CONCLUSION:The IL-6 -572 G/C and IL-8 3'-UTR 2767A/G polymorphisms are not associated with the risk of developing rheumatoid arthritis. However, the finding that patients with IL-8 3'-UTR 2767AA developed RA at a younger age suggests that this genotype may influence the etiopathology of RA in patients in Taiwan. Therefore, further single nucleotide polymorphism studies of this 3'UTR region may give more novel findings and understanding of the genetic basis of rheumatoid arthritis.     

Galectin-3 gene (<Emphasis Type="Italic">LGALS3</Emphasis>) +292C allele is a genetic predisposition factor for rheumatoid arthritis in Taiwan

Galectin-3 is a beta-galactoside-binding lectin which is involved in modulating inflammation and apoptosis. Elevated expression of galectin-3 has been demonstrated in synovium of rheumatoid arthritis (RA). The aim of our study is to investigate the genetic polymorphisms of galectin-3 in association with RA. Polymorphisms of galectin-3 gene (LGALS3) were compared between 151 RA patients and 182 healthy subjects in Taiwan. Variants at two LGALS3 single nucleotide polymorphism (SNP) sites (rs4644 and rs4652, corresponding to LAGLS3 +191 and +292) were genotyped by polymerase chain reaction (PCR) followed by restriction fragment length polymorphism (RFLP) and sequence-specific oligonucleotide probe hybridization, respectively. The allelic carriage of LGALS3 +292C was increased in patients with RA (66.9% in RA vs. 52.7% in controls, odds ratio = 1.8, 95% confidence interval = 1.2–2.8, p = 0.009). These results implicate that the genetic polymorphisms in galectin-3 gene may contribute to development of RA.