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银屑病关节炎患者红细胞糖基磷脂酰肌醇锚定膜CD59表达受损。与末端补体途径激活的关系。

Impaired expression of erythrocyte glycosyl-phosphatidylinositol-anchored membrane CD59 in patients with psoriatic arthritis. Relation to terminal complement pathway activation.

作者信息

Triolo G, Accardo-Palumbo A, Sallì L, Ciccia F, Ferrante A, Tedesco L, Sallì S, Giardina E, Pappalardo A, Licata G

机构信息

Department of Internal Medicine, Rheumatology and Clinical Immunology Unit, Division of Internal Medicine, Department of Pathology, University of Palermo, Italy.

出版信息

Clin Exp Rheumatol. 2003 Mar-Apr;21(2):225-8.

PMID:12747280
Abstract

OBJECTIVE

Complement-mediated injury is regulated by many factors; among these CD59 has been identified as a widely distributed glycoprotein that inhibits membrane C5b-9 (terminal complement component) formation. The aim of the study was to assess erythrocyte CD59 expression in patients with psoriatic arthritis in order to understand the role of CD59 in the pathogenesis.

METHODS

Washed erythrocytes from 50 patients with psoriatic arthritis, 8 with cutaneous psoriasis and 24 healthy subjects were incubated with monoclonal anti-CD59 antibody followed by a second FITC conjugated antibody and fluorescence intensity analysed by FAC-Scan flow cytometer to assess their CD59 membrane expression. SC5b-9 levels were measured in the plasma by ELISA and results compared with CD59 values. Immune complexes, complement C3 and C4 and rheumatoid factor were also determined.

RESULTS

Impaired expression of erythrocyte membrane-anchored CD59 was found in patients with psoriatic arthritis; the lowest levels were seen in active patients (p < 0.01). Increased SC5b-9 was seen in the plasma of patients with active disease. An inverse correlation was also found between plasma C5b-9 and the CD59 expression levels (r = -0.81, p < 0.001).

CONCLUSION

The low CD59 expression on erythrocytes from patients with psoriatic arthritis may be an index of a low tissue CD59 expression. This impairment could facilitate the activation of complement pathway and increase the risk for arthritis. Membrane attack complex formation in deficient membrane bound CD59 may also exacerbate synovial cell injury and inflammation.

摘要

目的

补体介导的损伤受多种因素调控;其中,CD59被鉴定为一种广泛分布的糖蛋白,可抑制膜C5b - 9(补体末端成分)的形成。本研究旨在评估银屑病关节炎患者红细胞CD59的表达,以了解CD59在发病机制中的作用。

方法

将50例银屑病关节炎患者、8例皮肤银屑病患者和24例健康受试者的洗涤红细胞与单克隆抗CD59抗体孵育,然后与第二种异硫氰酸荧光素(FITC)偶联抗体孵育,通过FAC - Scan流式细胞仪分析荧光强度,以评估其CD59膜表达。采用酶联免疫吸附测定法(ELISA)检测血浆中SC5b - 9水平,并将结果与CD59值进行比较。同时还测定了免疫复合物、补体C3和C4以及类风湿因子。

结果

银屑病关节炎患者红细胞膜锚定CD59表达受损;在活动期患者中水平最低(p < 0.01)。活动期疾病患者血浆中SC5b - 9升高。血浆C5b - 9与CD59表达水平之间也存在负相关(r = -0.81,p < 0.001)。

结论

银屑病关节炎患者红细胞上CD59低表达可能是组织CD59低表达的一个指标。这种损伤可能促进补体途径的激活,增加关节炎风险。膜结合CD59缺乏时膜攻击复合物的形成也可能加剧滑膜细胞损伤和炎症。

相似文献

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Impaired expression of erythrocyte glycosyl-phosphatidylinositol-anchored membrane CD59 in patients with psoriatic arthritis. Relation to terminal complement pathway activation.银屑病关节炎患者红细胞糖基磷脂酰肌醇锚定膜CD59表达受损。与末端补体途径激活的关系。
Clin Exp Rheumatol. 2003 Mar-Apr;21(2):225-8.
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CD59 efficiently protects human NT2-N neurons against complement-mediated damage.CD59能有效保护人类NT2-N神经元免受补体介导的损伤。
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[Glycosylphosphatidylinositol-anchored proteins with complement-regulatory activity on erythrocytes].[具有红细胞补体调节活性的糖基磷脂酰肌醇锚定蛋白]
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Levels of SC5b--9 complement complex in plasma and synovial fluid of patients with rheumatic disease.风湿性疾病患者血浆和滑液中SC5b-9补体复合物的水平。
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Generation of terminal complement complexes in psoriatic lesional skin.银屑病皮损皮肤中终末补体复合物的生成。
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Immunohistochemical determination of complement activation in joint tissues of patients with rheumatoid arthritis and osteoarthritis using neoantigen-specific monoclonal antibodies.使用新抗原特异性单克隆抗体对类风湿性关节炎和骨关节炎患者关节组织中的补体激活进行免疫组织化学测定。
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CD59: a molecule involved in antigen presentation as well as downregulation of membrane attack complex.CD59:一种参与抗原呈递以及膜攻击复合物下调的分子。
Exp Clin Immunogenet. 1992;9(1):33-47.

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