Association of IL-10 receptor 2 (IL10RB) SNP with systemic sclerosis

被引：37

作者：

Hikami, Koki ^{[1
]}

Ehara, Yukikazu ^{[2
]}

Hasegawa, Minoru ^{[3
]}

Fujimoto, Manabu ^{[3
]}

Matsushita, Masaki ^{[4
]}

Oka, Takanori ^{[4
]}

Takehara, Kazuhiko ^{[3
]}

Sato, Shinichi ^{[5
]}

Tokunaga, Katsushi ^{[2
]}

Tsuchiya, Naoyuki ^{[1
]}

机构：

[1] Univ Tsukuba, Doctoral Program Life Syst Med Sci, Grad Sch Comprehens Human Sci, Tsukuba, Ibaraki 3058575, Japan

[2] Univ Tokyo, Grad Sch Med, Dept Human Genet, Tokyo, Japan

[3] Kanazawa Univ, Dept Dermatol, Grad Sch Med Sci, Kanazawa, Ishikawa, Japan

[4] Wakunaga Pharmaceut Co Ltd, Hiroshima, Japan

[5] Nagasaki Univ, Dept Dermatol, Grad Sch Biomed Sci, Nagasaki 852, Japan

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2008年 / 373卷 / 03期

基金：

日本学术振兴会;

关键词：

systemic sclerosis; IL-10; receptor; polymorphism; genetics;

D O I：

10.1016/j.bbrc.2008.06.054

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Interleukin-10 (IL-10) signaling has been suggested to play a role in systemic sclerosis (SSc). IL10RB codes for IL-10 receptor 2 (IL-10R2), a component shared in receptor complexes for IL-10, IL-22, IL-26 and interferon (IFN)-gamma. In this study, we examined association of IL10RB polymorphism with susceptibility to SSc. Genotype A/A at rs2834167 (47K/K) was significantly increased in diffuse cutaneous SSc (dcSSc) (41.3% in dcSSc, 20.9% in controls, P= 0.0018, odds ratio = 2.67). A SNP in the 5' flanking region of IL10RB, rs999788, also showed association with dcSSc; however, this association was shown to be secondarily caused by linkage disequilibrium with rs2834167. Significant association was not observed in limited cutaneous SSc (1cSSc). Presence of anti-topoisomerase I antibody was also associated with rs2834167A/A genotype (P=0.0019). Serum IL-10 level was significantly associated with the number of rs2834167A allele (P=0.007). These findings suggested that signaling through IL-10R2 may play a causative role in dcSSc. (c) 2008 Elsevier Inc. All rights reserved.

引用

页码：403 / 407

页数：5

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