Changes in synovial tissue Jak-STAT expression in rheumatoid arthritis in response to successful DMARD treatment
Changes in synovial tissue Jak-STAT expression in rheumatoid arthritis in response to successful DMARD treatment
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DOI：
10.1136/ard.2005.050385
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发表时间：
2006-12-01
影响因子：
27.4
通讯作者：
Smith, M. D.
中科院分区：
文献类型：
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作者：
Walker, J. G.;Ahern, M. J.;Smith, M. D.
背景：JAK-STAT信号的调节可能为炎症性关节炎(IA)提供一种有效的治疗策略。目的：探讨抗风湿药物(DMARD)治疗成功对活动期类风湿关节炎(RA)患者滑膜组织中JAK-STAT表达的影响。方法：采用免疫组织化学方法检测16例活动期类风湿关节炎患者在DMARD治疗前后滑膜组织中JAK-STAT 3、信号转导和转录激活因子(STAT)1、STAT4和STAT6的表达。结果：DMARD治疗成功后，类风湿关节炎滑膜组织中STAT1表达减少，STAT1和STAT6表达减少。虽然DMARD治疗后STAT4和JAK3的总体表达没有明显改变，但被认为是激活的树突状细胞亚群的STAT4和JAK3明亮细胞的表达显著减少。结论：结果表明，标准DMARD治疗类风湿关节炎成功后，JAK3、STAT1、STAT4和STAT6亚单位的表达减少。因此，改变这些途径的表达可能代表着另一种治疗选择，要么通过促进抑制途径的上调，要么通过抑制炎症途径。
Background: Modulation of Jak-STAT signalling may provide an effective therapeutic strategy in inflammatory arthritis (IA). Objective: To examine the effect of successful disease-modifying antirheumatic drug (DMARD) treatment on the expression of Jak-STAT in a cohort of patients with active rheumatoid arthritis.Methods: Synovial tissue biopsy specimens from 16 patients with active rheumatoid arthritis, taken before and after initiation of DMARD treatment, were examined for the presence of janus kinase (Jak) 3, signal transducer and activator of transcription (STAT) 1, STAT4 and STAT6 expression using immunohistochemistry.Results: Successful treatment with DMARDs results in reduction in STAT1 expression in the lining, and STAT1 and STAT6 in the sublining of rheumatoid arthritis synovial tissue. Although the overall expression of STAT4 and Jak3 was not significantly altered by DMARD treatment, there was a significant reduction in the expression of the STAT4 and Jak3 bright cells, thought to be an activated dendritic cell subpopulation.Conclusion: Results show that Jak3, STAT1, STAT4 expression and STAT6 sublining expression decrease in response to successful treatment of rheumatoid arthritis with standard DMARDs. Therefore, altering the expression of these pathways may represent an alternative treatment option, either through promoting upregulation of inhibitory pathways, or suppressing inflammatory paths.