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Antibody glycosylation as a potential biomarker for chronic inflammatory autoimmune diseases

机译:抗体糖基化是慢性炎性自身免疫疾病的潜在生物标志物

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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-Sch?nlein purpura.
机译:已知免疫球蛋白(Ig)的糖基化会在生理和病理条件下影响其效应子功能。多年来研究了各种炎性自身免疫疾病中免疫球蛋白G和自身抗体的糖基化模式变化。然而,尽管进行了广泛的研究,例如,关于这种差异糖基化抗体的形成以及其他免疫球蛋白类别中糖基化模式的改变,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。已经显示,Ig糖基化模式的改变在疾病发作之前出现,而且可以接受治疗。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的生物标志物或监测慢性炎症性自身免疫疾病(如抗磷脂综合征,类风湿性关节炎,系统性红斑狼疮,ANCA相关性脉管炎和过敏性紫癜性紫癜)的潜力。 。

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