FcRL3 and multiple sclerosis pathogenesis:: Role in autoimmunity?

被引:24
作者
Martinez, Alfonso
Mas, Ana
de las Heras, Virginia
Bartolome, Manuel
Arroyo, Rafael
Fernandez-Arquero, Miguel
de la Concha, Emilio G.
Urcelay, Elena
机构
[1] Hosp Clin San Carlos, Dept Immunol, E-28040 Madrid, Spain
[2] Hosp Clin San Carlos, Dept Neurol, Madrid, Spain
关键词
FcRL3; polymorphism; multiple sclerosis; genetic susceptibility; FC-GAMMA-RIIA; SYSTEMIC-LUPUS-ERYTHEMATOSUS; RHEUMATOID-ARTHRITIS; GENETIC ASSOCIATION; RECEPTOR; POLYMORPHISMS; SUSCEPTIBILITY; DELETION; COLLAGEN; MODEL;
D O I
10.1016/j.jneuroim.2007.06.018
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Background and aims: A functional promoter polymorphism in the FcPL3 gene, - 169 T/C, has been shown to regulate gene expression and to play a role in several autoimmune diseases. We aimed at testing for the first time whether this gene was involved in multiple sclerosis (MS) pathogenesis. Methods: Case-control study performed with 400 Spanish MS patients and 508 healthy subjects. Genotyping of - 169 T/C and - 110 G/A was ascertained by using TaqMan MGB chemistry following manufacturer suggestions (Applied Biosystems, CA, USA). Results: As previously seen for other autoimmune diseases, a significant difference was observed in the distribution of - 169 T/C FcRL3 genotypes between MS patients and healthy controls (p=0.03; chi(2)=6.99). The - 169 T allele, recently associated with increased susceptibility to Addison's disease, showed a parallel effect in MS [(TT+TC) vs. CC: p=0.013; OR= 1.55 (1.08-2.54)]. Conclusions: An increased susceptibility associated to the - 169 T allele was found when MS patients and controls were compared, supporting the role of the FcRL3 locus in MS predisposition and therefore extending the evidence of its general influence on autoimmunity. (C) 2007 Elsevier B.V. All rights reserved.
引用
收藏
页码:132 / 136
页数:5
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