Bankó Zsuzsanna, Pozsgay Judit, Gáti Tamás, Rojkovich Bernadette, Ujfalussy Ilona, Sármay Gabriella
Department of Immunology, Eötvös Loránd University, Pázmány Péter sétány 1/c, Budapest 1117, Hungary.
Buda Hospital of Hospitaller Brothers of St. John, Frankel Leó út 17-19, Budapest 1027, Hungary.
Clin Immunol. 2017 Nov;184:63-69. doi: 10.1016/j.clim.2017.05.012. Epub 2017 May 12.
Cytokines, including tumor necrosis factor alpha (TNFα) 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.
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.
细胞因子，包括肿瘤坏死因子α（TNFα），通过增强自身免疫、维持滑膜长期炎症以及促进关节损伤参与类风湿性关节炎（RA）的发病机制。抗TNF治疗是RA最有效且应用最广泛的治疗方法之一，尽管其机制尚未阐明。我们之前证明，与健康个体相比，RA患者产生白细胞介素-10的调节性B细胞（B10细胞）数量减少且功能受损。我们的目的是研究抗TNF治疗对RA患者B10细胞的影响，追踪B细胞活化标志物（CD25、CD69）的变化，并监测治疗期间患者血清中瓜氨酸化肽特异性抗体水平和分泌的白细胞介素-10水平。我们观察到，在开始治疗六个月后，B10细胞频率显著增加，而B细胞上活化标志物CD69的表达降低。相比之下，治疗后血清中白细胞介素-10和抗瓜氨酸化肽抗体水平没有变化。
B细胞活化状态降低以及调节性B10细胞数量增加可能有助于抗TNF药物对RA的治疗效果。
