Regulatory B cells in rheumatoid arthritis: Alterations in patients receiving anti-TNF therapy
Regulatory B cells in rheumatoid arthritis: Alterations in patients receiving anti-TNF therapy
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DOI：
10.1016/j.clim.2017.05.012
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发表时间：
2017-11-01
影响因子：
8.6
通讯作者：
Sarmay, Gabriella
中科院分区：
文献类型：
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作者：
Banko, Zsuzsanna;Pozsgay, Judit;Sarmay, Gabriella
包括肿瘤坏死因子α (TNF α)在内的细胞因子通过增强自身免疫、维持滑膜长期炎症和促进关节损伤参与类风湿关节炎（RA）的发病过程。抗肿瘤坏死因子治疗是治疗类风湿性关节炎最有效、应用最广泛的治疗方法之一，但其机制尚不明确。先前我们证明，与健康个体相比，RA患者产生IL-10的调节性B细胞（B10细胞）数量减少，并且功能受损。我们的目的是研究抗tnf治疗对RA患者B10细胞的影响，跟踪B细胞活化标志物（CD25, CD69）的变化，监测治疗期间患者血清中瓜氨酸肽特异性抗体水平和分泌IL-10水平。我们观察到，在开始治疗6个月后，B10细胞的频率显著增加，而激活标记物CD69在B细胞上的表达减少。相比之下，血清IL-10和抗瓜氨酸肽抗体水平在治疗后没有变化。结论：B细胞活化状态降低，调节性B10数量增加。细胞可能有助于抗肿瘤坏死因子药物治疗RA的疗效。(C) 2017爱思唯尔公司版权所有。
Cytokines, including tumor necrosis factor alpha (TNF alpha) are involved in Rheumatoid arthritis (RA) pathogenesis by augmenting autoimmunity, sustaining long term inflammation in the synovium, and promoting joint damage. Anti-TNF therapy is one of the most efficient and widely used therapies for RA, although its mechanism is not clarified yet. Earlier we demonstrated that RA patients have a reduced number of IL-10 producing regulatory B cells (B10 cells) as compared to healthy individuals and they are functionally impaired. Our aim was to study the influence of anti-TNF therapy on B10 cells in RA, to follow the alteration of B cell activation markers (CD25, CD69) and to monitor the level of citrullinated peptid-specific antibodies and the secreted IL-10 in patients' sera during the therapy.We have observed that at six month after starting the therapy the frequency of B10 cells remarkably increased, while the expression of the activation marker, CD69 decreased on B cells. In contrast, serum levels of IL-10 and anti-citrullinated peptide antibodies did not change post-treatment.Conclusion: The reduced activation state of B cells and the increasing number of regulatory B10. cells might contribute to the therapeutic efficacy of anti-TNF agents in RA. (C) 2017 Elsevier Inc. All rights reserved.