Th2-mediated atopic disease protection in Th1-mediated rheumatoid arthritis.

Th2-mediated atopic disease protection in Th1-mediated rheumatoid arthritis.
复制标题

Th2 介导的特应性疾病对 Th1 介导的类风湿性关节炎的保护作用。

DOI:
--
复制
发表时间:
2003
影响因子:
3.7
通讯作者:
G. Bein
G. Bein
中科院分区:
医学4区
文献类型:
--
作者:
Hartung Ad;A. Bohnert;H. Hackstein;A. Ohly;Schmidt Kl;G. Bein

文献摘要

被引文献

相似文献

目的 CD4 + T辅助细胞亚群(Th1和Th2)之间的平衡在类风湿关节炎(RA)和特应性疾病的发病机制中起着重要作用。虽然RA被认为是Th1介导的疾病,但Th2细胞在特应性疾病中占主导地位。本研究的目的是调查类风湿关节炎患者和对照组在过敏、花粉热、屋尘螨敏感性和哮喘以及血清总IgE水平方面的差异。 方法 在134例RA患者中评估了特应性疾病的病史,并与305例健康献血者进行了比较。RA患者还回答了有关疾病活动性和严重程度的临床问题。考虑到疾病改善治疗,测量两组的血清总IgE水平。 结果 与对照组相比,类风湿关节炎患者中花粉热病史(2.3%)和屋尘螨敏感性(3.1%)的发生率显著降低(分别为24.2%和12.2%; p <0.0001和p <0.003)。此外,RA患者血清总IgE水平显著低于对照组(p <0.0001)。与非特应性RA患者相比,特应性RA患者的严重程度较低。 结论 这些结果支持RA和特应性相互拮抗的概念,Th1和Th2细胞的细胞因子模式的变化可以提供对RA疗效的指示。
OBJECTIVE The balance between CD4+ T-helper (h) cell subsets (Th1 and Th2) plays an important role in the pathogenesis of rheumatoid arthritis (RA) and atopy. While RA is believed to be a Th1 mediated disease, Th2 cells predominate in atopic disorders. The purpose of this study was to investigate differences in the occurrence of allergy, hay fever, house dust mite sensitivity and asthma, as well as total serum IgE levels in RA patients and controls. METHODS The case history of atopic disorders was assessed in 134 RA patients and compared to those found in 305 healthy blood donors. RA patients also answered clinical questions concerning disease activity and severity. Total serum IgE levels were measured in both groups, taking into consideration disease modifying therapy. RESULTS A significantly lower occurrence of medical history of hay fever (2.3%) and house dust mite sensitivity (3.1%) was found among RA patients compared to controls (24.2% and 12.2%, respectively; p < 0.0001 and p < 0.003 respectively). Moreover, RA patients had significantly lower total serum IgE levels than control subjects (p < 0.0001). RA was less severe in patients with atopy compared to non-atopic RA patients. CONCLUSION These results support the concept that RA and atopy antagonize each other and that a change in the cytokine patterns of Th1 and Th2 cells could provide an indication for curative effects on RA.