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类风湿关节炎中转化生长因子β1基因多态性

Transforming growth factor beta1 gene polymorphism in rheumatoid arthritis.

作者信息

Sugiura Y, Niimi T, Sato S, Yoshinouchi T, Banno S, Naniwa T, Maeda H, Shimizu S, Ueda R

机构信息

Second Department of Internal Medicine, Nagoya City University, Medical School, Nagoya, Japan.

出版信息

Ann Rheum Dis. 2002 Sep;61(9):826-8. doi: 10.1136/ard.61.9.826.

DOI:10.1136/ard.61.9.826
PMID:12176809
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1754235/
Abstract

OBJECTIVE

Rheumatoid arthritis (RA) is a chronic inflammatory disease and synovial cells, antigen presenting cells, lymphocytes, and their cytokines might be associated with the disease. Transforming growth factor beta1 (TGFbeta1) has been reported to have important roles in unresolved inflammation, immune suppression, fibrosing processes, and angiogenesis. TGFbeta1 is highly expressed in joints in RA and is considered to be a regulator of anti-inflammation in RA. Polymorphisms of TGFbeta1 have been reported to be associated with the production of TGFbeta1 protein, and to increase the risk of acquiring several diseases. It was speculated that these polymorphisms might also be involved in RA, and therefore the TGFbeta1 codon 10 T869C polymorphism in a series of patients and controls was investigated.

METHOD

A total of 155 patients with RA and 110 healthy subjects were studied. DNA was extracted from peripheral leucocytes and TGFbeta1 codon 10 T869C polymorphism was determined by polymerase chain reaction restriction fragment polymorphism.

RESULTS

A significantly higher proportion of patients with RA with the T allele (CT type or TT type) was found compared with the CC type (p=0.039).

CONCLUSION

The T allele, previously reported to be linked with production of TGFbeta1, may be associated with an increased risk of RA.

摘要

目的

类风湿性关节炎(RA)是一种慢性炎症性疾病,滑膜细胞、抗原呈递细胞、淋巴细胞及其细胞因子可能与该疾病有关。据报道,转化生长因子β1(TGFβ1)在持续性炎症、免疫抑制、纤维化过程和血管生成中起重要作用。TGFβ1在RA患者的关节中高表达,被认为是RA抗炎的调节因子。据报道,TGFβ1的多态性与TGFβ1蛋白的产生有关,并增加患几种疾病的风险。推测这些多态性也可能与RA有关,因此对一系列患者和对照中的TGFβ1密码子10 T869C多态性进行了研究。

方法

共研究了155例RA患者和110例健康受试者。从外周血白细胞中提取DNA,通过聚合酶链反应-限制性片段多态性测定TGFβ1密码子10 T869C多态性。

结果

与CC型相比,发现携带T等位基因(CT型或TT型)的RA患者比例显著更高(p = 0.039)。

结论

先前报道与TGFβ1产生相关的T等位基因可能与RA风险增加有关。