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类风湿关节炎中滑膜组织Jak-STAT表达对成功的改善病情抗风湿药治疗的反应变化。

Changes in synovial tissue Jak-STAT expression in rheumatoid arthritis in response to successful DMARD treatment.

作者信息

Walker J G, Ahern M J, Coleman M, Weedon H, Papangelis V, Beroukas D, Roberts-Thomson P J, Smith M D

机构信息

Repatriation General, Hospital, Daws Road, Daw Park 5041, South Australia, Australia.

出版信息

Ann Rheum Dis. 2006 Dec;65(12):1558-64. doi: 10.1136/ard.2005.050385. Epub 2006 Jun 7.

DOI:10.1136/ard.2005.050385
PMID:16760256
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1798468/
Abstract

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 up-regulation of inhibitory pathways, or suppressing inflammatory paths.

摘要

背景

调节Jak-STAT信号通路可能为炎性关节炎（IA）提供一种有效的治疗策略。

目的

研究成功使用改善病情抗风湿药（DMARD）治疗对一组活动性类风湿关节炎患者Jak-STAT表达的影响。

方法

采用免疫组织化学法检测16例活动性类风湿关节炎患者在DMARD治疗前后滑膜组织活检标本中janus激酶（Jak）3、信号转导及转录激活因子（STAT）1、STAT4和STAT6的表达情况。

结果

DMARDs成功治疗可使类风湿关节炎滑膜组织衬里层的STAT1表达以及滑膜下层的STAT1和STAT6表达降低。尽管DMARD治疗未显著改变STAT4和Jak3的总体表达，但被认为是活化树突状细胞亚群的STAT4和Jak3高表达细胞的表达显著降低。

结论

结果表明，标准DMARDs成功治疗类风湿关节炎后，Jak3、STAT1、STAT4表达及STAT6滑膜下层表达降低。因此，改变这些信号通路的表达可能代表一种替代治疗选择，可通过促进抑制性通路的上调或抑制炎性通路来实现。

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本文引用的文献

1
The Jak-STAT pathway in rheumatoid arthritis.类风湿关节炎中的Jak-STAT信号通路。
J Rheumatol. 2005 Sep;32(9):1650-3.
2
Inhibition of inflammatory bone erosion by constitutively active STAT-6 through blockade of JNK and NF-kappaB activation.通过阻断JNK和NF-κB激活，组成型活性STAT-6抑制炎症性骨侵蚀。
Arthritis Rheum. 2005 Sep;52(9):2719-29. doi: 10.1002/art.21286.
3
Expression of Jak3, STAT1, STAT4, and STAT6 in inflammatory arthritis: unique Jak3 and STAT4 expression in dendritic cells in seropositive rheumatoid arthritis.Jak3、STAT1、STAT4和STAT6在炎性关节炎中的表达：血清阳性类风湿关节炎中树突状细胞独特的Jak3和STAT4表达。
Ann Rheum Dis. 2006 Feb;65(2):149-56. doi: 10.1136/ard.2005.037929. Epub 2005 Aug 11.
4
Targeting the Jak/STAT pathway for immunosuppression.靶向Jak/STAT通路进行免疫抑制。
Ann Rheum Dis. 2004 Nov;63 Suppl 2(Suppl 2):ii67-ii71. doi: 10.1136/ard.2004.028290.
5
Signaling by STATs.信号转导与转录激活因子（STATs）介导的信号传导
Arthritis Res Ther. 2004;6(4):159-68. doi: 10.1186/ar1197. Epub 2004 Jun 21.
6
Local activation of STAT-1 and STAT-3 in the inflamed synovium during zymosan-induced arthritis: exacerbation of joint inflammation in STAT-1 gene-knockout mice.在酵母聚糖诱导的关节炎中，炎症滑膜中STAT-1和STAT-3的局部激活：STAT-1基因敲除小鼠关节炎症的加剧
Arthritis Rheum. 2004 Jun;50(6):2014-23. doi: 10.1002/art.20302.
7
Activation of the STAT1 pathway in rheumatoid arthritis.类风湿关节炎中STAT1信号通路的激活
Ann Rheum Dis. 2004 Mar;63(3):233-9. doi: 10.1136/ard.2003.013276.
8
Rheumatoid arthritis is a heterogeneous disease: evidence for differences in the activation of the STAT-1 pathway between rheumatoid tissues.类风湿性关节炎是一种异质性疾病：类风湿组织中STAT-1通路激活存在差异的证据。
Arthritis Rheum. 2003 Aug;48(8):2132-45. doi: 10.1002/art.11096.
9
Evolving concepts of rheumatoid arthritis.类风湿关节炎的概念演变
Nature. 2003 May 15;423(6937):356-61. doi: 10.1038/nature01661.
10
NF-kappa B in rheumatoid arthritis: a pivotal regulator of inflammation, hyperplasia, and tissue destruction.类风湿关节炎中的核因子κB：炎症、增生及组织破坏的关键调节因子
Arthritis Res. 2001;3(4):200-6. doi: 10.1186/ar300. Epub 2001 Mar 26.