抗体糖基化作为慢性炎症性自身免疫性疾病的潜在生物标志物

J. Knopf, Mona H. C. Biermann, L. Munoz, M. Herrmann
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引用次数: 5

摘要

免疫球蛋白(Ig)的糖基化在生理和病理条件下影响其效应功能。免疫球蛋白G和自身抗体在各种炎症性自身免疫性疾病中糖基化模式的变化已被研究多年。然而,尽管进行了广泛的研究,但关于这种差异糖基化抗体的形成和其他免疫球蛋白类糖基化模式的改变,许多问题仍然难以捉摸。然而,知识已经大大加深,特别是在类风湿关节炎领域。Ig糖基化模式的改变已被证明出现在发病前,而且可以受到治疗。在这篇综述中,我们讨论了检测Ig糖基化变化作为疾病活动性或监测慢性炎症性自身免疫性疾病(如抗磷脂综合征、类风湿性关节炎、系统性红斑狼疮、anca相关血管炎和Henoch-Schönlein紫癜)患者的生物标志物的潜力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Antibody glycosylation as a potential biomarker for chronic inflammatory autoimmune diseases
Abstract Glycosylation of immunoglobulins (Ig) is known to influence their effector functions in physiological and pathological conditions. Changes in the glycosylation pattern of immunoglobulin G and autoantibodies in various inflammatory autoimmune diseases have been studied for many years. However, despite extensive research, many questions are still elusive regarding the formation of such differentially glycosylated antibodies and alterations of glycosylation patterns in other immunoglobulin classes for example. Nevertheless, knowledge has been deepened greatly, especially in the field of rheumatoid arthritis. Changes of Ig glycosylation patterns have been shown to appear before onset of the disease and moreover can subject to treatment. In this review, we discuss the potential of detecting Ig glycosylation changes as biomarkers for disease activity or monitoring of patients with chronic inflammatory autoimmune diseases such as antiphospholipid syndrome, rheumatoid arthritis, systemic lupus erythematosus, ANCA-associated vasculitis and Henoch-Schönlein purpura.
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AIMS Genetics
AIMS Genetics GENETICS & HEREDITY-
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