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B 细胞在强直性脊柱炎发病机制中的作用。

B Cell Involvement in the Pathogenesis of Ankylosing Spondylitis.

机构信息

Department of Rheumatology and Clinical Immunology, University of Groningen, University Medical Center Groningen, Hanzeplein 1, 9713 GZ Groningen, The Netherlands.

出版信息

Int J Mol Sci. 2021 Dec 11;22(24):13325. doi: 10.3390/ijms222413325.

DOI:10.3390/ijms222413325
PMID:34948121
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8703482/
Abstract

Extensive research into ankylosing spondylitis (AS) has suggested the major role of genetics, immune reactions, and the joint-gut axis in its etiology, although an ultimate consensus does not yet exist. The available evidence indicates that both autoinflammation and T-cell-mediated autoimmune processes are actively involved in the disease process of AS. So far, B cells have received relatively little attention in AS pathogenesis; this is largely due to a lack of conventional disease-defining autoantibodies. However, against prevailing dogma, there is a growing body of evidence suggestive of B cell involvement. This is illustrated by disturbances in circulating B cell populations and the formation of auto-reactive and non-autoreactive antibodies, along with B cell infiltrates within the axial skeleton of AS patients. Furthermore, the depletion of B cells, using rituximab, displayed beneficial results in a subgroup of patients with AS. This review provides an overview of our current knowledge of B cells in AS, and discusses their potential role in its pathogenesis. An overarching picture portrays increased B cell activation in AS, although it is unclear whether B cells directly affect pathogenesis, or are merely bystanders in the disease process.

摘要

对强直性脊柱炎(AS)的广泛研究表明,遗传、免疫反应和关节-肠道轴在其发病机制中起主要作用,尽管尚未达成最终共识。现有证据表明,自身炎症和 T 细胞介导的自身免疫过程都积极参与了 AS 的疾病过程。到目前为止,B 细胞在 AS 发病机制中的研究相对较少;这主要是由于缺乏传统的疾病定义性自身抗体。然而,与流行的观点相反,越来越多的证据表明 B 细胞参与其中。这体现在循环 B 细胞群的紊乱、自身反应性和非自身反应性抗体的形成,以及 AS 患者的轴性骨骼中的 B 细胞浸润。此外,使用利妥昔单抗清除 B 细胞在亚组 AS 患者中显示出有益的结果。这篇综述提供了我们目前对 AS 中 B 细胞的认识概述,并讨论了它们在发病机制中的潜在作用。一个总体的描述是,AS 中 B 细胞的激活增加,尽管尚不清楚 B 细胞是否直接影响发病机制,还是仅仅是疾病过程中的旁观者。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3ec/8703482/49db84501750/ijms-22-13325-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3ec/8703482/28fce959ccc1/ijms-22-13325-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3ec/8703482/49db84501750/ijms-22-13325-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3ec/8703482/28fce959ccc1/ijms-22-13325-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3ec/8703482/49db84501750/ijms-22-13325-g002.jpg

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