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B 细胞和自身抗体在强直性脊柱炎中的潜在作用。

Potential Roles for B cells and Autoantibodies in Ankylosing Spondylitis.

机构信息

Rheumatology Research Center, Tehran University of Medical Sciences, Tehran, Iran.

Research Center for Chronic Inflammatory Diseases, Tehran University of Medical Sciences, Tehran, Iran.

出版信息

Curr Rheumatol Rev. 2024;20(2):157-164. doi: 10.2174/0115733971243468231012044909.

DOI:10.2174/0115733971243468231012044909
PMID:37870058
Abstract

Ankylosing spondylitis (AS) is a chronic inflammatory rheumatic disease that predominantly affects young males. AS is a condition in which the spine and sacroiliac joints become inflamed. More specifically, most AS patients experience spine malformations over time, resulting in functional incapability. The etiopathogenesis of AS is a complex combination of genetic predisposition and environmental factors. Extensive studies on AS have revealed the central role of genetics and immune reactions in its etiology. However, an utmost agreement has yet to be created. The available evidence suggests that both autoinflammation and T-cell-mediated autoimmune processes have significant roles in the disease process of AS. So far, B cells have obtained moderately little attention in AS pathogenesis, primarily because of the absence of disease-defining autoantibodies. However, against general dogma, evidence is mounting showing B cell involvement. Disruptions depict this in circulating B cell populations, the increased expression of immunoglobulin (Ig)G, IgA, and IgM, and B cell infiltration within the axial skeleton of AS patients. Meanwhile, compared to many other inflammatory autoimmune disorders, AS has no disease-specific autoantibodies that help disease diagnosis. This study has provided an overview of the B lymphocytes and antibodies' role in AS pathogenesis. It also introduces autoantibodies that can be the prognosis and diagnosis biomarkers of AS.

摘要

强直性脊柱炎(AS)是一种主要影响年轻男性的慢性炎症性风湿病。AS 是一种脊柱和骶髂关节发炎的疾病。更具体地说,大多数 AS 患者随着时间的推移会出现脊柱畸形,导致功能丧失。AS 的发病机制是遗传易感性和环境因素的复杂组合。对 AS 的广泛研究揭示了遗传和免疫反应在其发病机制中的核心作用。然而,尚未达成最终共识。现有证据表明,自身炎症和 T 细胞介导的自身免疫过程在 AS 的发病过程中都具有重要作用。到目前为止,B 细胞在 AS 发病机制中的作用受到的关注较少,主要是因为缺乏疾病定义性的自身抗体。然而,与普遍观点相反,越来越多的证据表明 B 细胞参与其中。这表现在循环 B 细胞群的紊乱、免疫球蛋白(Ig)G、IgA 和 IgM 的表达增加以及 AS 患者的轴性骨骼中的 B 细胞浸润。同时,与许多其他炎症性自身免疫性疾病相比,AS 没有有助于疾病诊断的特异性自身抗体。本研究概述了 B 淋巴细胞和抗体在 AS 发病机制中的作用。它还介绍了可以作为 AS 预后和诊断生物标志物的自身抗体。

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