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Association of IL-10 receptor 2 (IL10RB) SNP with systemic sclerosis |
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| Authors: | Hikami Koki Ehara Yukikazu Hasegawa Minoru Fujimoto Manabu Matsushita Masaki Oka Takanori Takehara Kazuhiko Sato Shinichi Tokunaga Katsushi Tsuchiya Naoyuki |
| Institution: | a Doctoral Program in Life System Medical Sciences, Graduate School of Comprehensive Human Sciences, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki 305-8575, Japan b Department of Human Genetics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan c Department of Dermatology, Kanazawa University, Graduate School of Medical Science, Kanazawa, Japan d Wakunaga Pharmaceutical Co., Ltd., Hiroshima, Japan e Department of Dermatology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan |
| Abstract: | 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)-λ. 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 (lcSSc). 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. |
| Keywords: | Systemic sclerosis IL-10 receptor Polymorphism Genetics |
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