The polymorphism C5507G of complement receptor 1 does not explain idiopathic pulmonary fibrosis among the Finns

被引:13
作者
Hodgson, U
Tukiainen, P
Laitinen, T
机构
[1] Univ Helsinki Hosp, Pulm Clin, Dept Pulm Med, Helsinki 00029, Finland
[2] Univ Helsinki, Dept Med Genet, FIN-00014 Helsinki, Finland
基金
芬兰科学院;
关键词
pulmonary fibrosis; genetics;
D O I
10.1016/j.rmed.2004.08.003
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Idiopathic pulmonary fibrosis is the most common of the idiopathic interstitial lung diseases referring to the histo-pathological entity of usual interstitial pneumonia. It has been hypothesized that inflammation may trigger the multiformic fibrotic lesions found in the affected lung, and defects in the innate immune defense, including the complement, can predispose to pulmonary fibrosis. The polymorphism C5507G in the Complement Receptor 1 gene has been recently associated with idiopathic pulmonary fibrosis. C5507G causes an amino acid change from proline to arginine, and opens a potential cleavage site for trypsin-like enzymes and, therefore, a potential mechanism for increased shedding of the molecule from the cell surface. We studied the polymorphism in 96 Finnish patients with idiopathic pulmonary fibrosis and 164 population based controls. ALL the patients and controls were C5507 homozygous suggesting that either the Finns do not carry the G5507 polymorphism or it is extremely rare. We conclude that G5507 is not a susceptibility allele for idiopathic pulmonary fibrosis among Finnish patients. (C) 2004 Elsevier Ltd. All rights reserved.
引用
收藏
页码:265 / 267
页数:3
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