Soluble tumour necrosis factor receptor treatment does not affect raised transforming growth factor β levels in rheumatoid arthritis

Soluble tumour necrosis factor receptor treatment does not affect raised transforming growth factor β levels in rheumatoid arthritis
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DOI:
10.1136/ard.61.3.254
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发表时间:
2002-03-01
影响因子:
27.4
通讯作者:
Kekow, J
Kekow, J
中科院分区:
医学1区
文献类型:
--
作者:
Drynda, S;Kühne, C;Kekow, J

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目的:通过研究依那西普治疗后类风湿关节炎(RA)患者血浆转化生长因子β1(TGFbeta)水平的变化,进一步阐明抗肿瘤坏死因子α治疗类风湿关节炎(RA)的免疫调节作用。方法:检测26例RA患者治疗6个月后血浆TGFbeta1、TGFbeta2水平,并与病情活动度及实验室指标包括基质金属蛋白酶-3(MMP3)、白介素6(IL6)进行比较。治疗过程中IL6、MMP3水平明显下降,同时血清标志物(C反应蛋白、血沉)和临床疾病活动度(视觉模拟评分、Thompson关节评分)下降。相比之下,在整个六个月中,所有样本中潜伏的TGFbeta1水平都很高。结论:依那西普治疗可引起细胞因子网络的细微变化。尽管促炎细胞因子IL6被下调,但高水平的TGFβ血浆水平的持续存在表明在RA中存在尚不清楚的TGFβ过度表达的机制。这可能导致严重的感染,并可能导致肿瘤防御系统的改变。
Objective: To further elucidate the immunomodulating effects of anti-tumour necrosis factor a treatment in rheumatoid arthritis (RA) by studying changes in plasma levels of transforming growth factor beta (TGFbeta) in patients with RA undergoing etanercept treatment.Methods: Plasma levels of TGFbeta1 and TGFbeta2 were determined in 26 patients with RA during six months of etanercept treatment and compared with disease activity and laboratory parameters, including matrix metalloproteinase-3 (MMP-3) and interleukin 6 (IL6).Results: Before treatment all patients had raised TGFbeta1, IL6, and MMP-3 levels. In the course of treatment IL6 and MMP-3 levels decreased significantly, accompanied by a drop in serological markers (C reactive protein and erythrocyte sedimentation rate) and clinical disease activity (visual analogue scale and Thompson joint score). By contrast, high levels of latent TGFbeta1 were present in all specimens over the entire six months. TGFbeta2 levels did not change during treatment.Conclusions: Etanercept treatment induces subtle changes in the cytokine network. Although the proinflammatory cytokine IL6 is down regulated, the persistence of high TGFbeta plasma levels indicates the existence of as yet unknown mechanisms for TGFbeta overexpression in RA. This may predispose to severe infections and can cause an altered tumour defence.