Contribution of LILRB1 polymorphism and HLA-DRB1-shared epitope to rheumatoid arthritis

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• 作者：Juan Francisco Delgado De La Poza^a ; Elisabet Cantó ; ^b ; C&#233 ; sar Dí ; az-Torn&#233 ; ^c ; Beatriz Ferrer Villahoz^b ; M. Angeles Martí ; nez Carretero^a ; Marta Ló ; pez^a ; Carmen Geli^c ; C&#233 ; sar Dí ; az^c ; Jos&#233 ; Luis Rodrí ; guez-Sá ; nchez^a ; Silvia Vidal^b ; ^{svidal@santpau.cat}
• 关键词：LILRB1 ; Arthritis ; Polymorphism
• 刊名：Inmunolog铆a
• 出版年：2011
• 期刊代码：pca191_02139626
• 类别：med
• 出版时间：October鈥揇ecember 2011
• 卷：30
• 期：4
• 页码：108-114
• 文件大小：324 K

摘要

lass="h4">Objectives

The LILRB1 gene has recently been associated with rheumatoid arthritis (RA) susceptibility in HLA-DRB1-shared epitope (SE) negative Japanese individuals. Since the contribution of the LILRB1 polymorphism to RA susceptibility may vary among ethnic populations, we examined this association in a group of Caucasian patients. The frequency of LILRB1 alleles was also determined in patients according to the presence of DRB1-SE.

lass="h4">Methods

Samples from 103 RA patients and 107 healthy controls were randomly collected. Polymorphism of the LILRB1 gene was analyzed by sequencing with primers that amplified intron 3 and exon 4.

lass="h4">Results

The frequencies of LILRB1 alleles in RA patients did not differ from those of controls. However, when patients and controls were grouped according to SE, the PE-01/01 genotype was less frequent in negative-SE patients than in controls. Whereas SE is associated with higher anti-CCP antibody levels, as expected, the production of anti-CCP antibodies was lower in negative-SE patients with PE-01/01 genotype. Moreover, radiographic damage in hand and feet of SE-negative PE-01/01 patients was less severe than in patients with other genotypes.

lass="h4">Conclusions

The participation of this LILRB1 polymorphism in the RA pathogenesis of this Caucasian cohort differed from that reported in a Japanese sample. Our findings suggest that the LILRB1-PE-01/01 genotype could exert a protective role in RA susceptibility and disease severity in the absence of SE.