Biochemical and Biophysical Research Communications
Association of IL-10 receptor 2 (IL10RB) SNP with systemic sclerosis
Section snippets
Materials and methods
Patients and controls. Forty-six patients with dcSSc (10 males and 36 females, average age 47.5 ± 16.1 years), 78 patients with lcSSc (4 males and 74 females, average age 54.8 ± 10.8 years), and healthy controls (229 males and 169 females, 28.6 ± 7.3 years) were studied. SSc was classified according to the American College of Rheumatology criteria [20]. Patients and healthy controls were recruited at Kanazawa University, The University of Tokyo and associated laboratories. All patients and healthy
Association of IL10RB E47 K with dcSSc
We initially focused on IL10RB rs2834167 coding for a nonsynonymous substitution E47K, because this SNP was associated with other conditions [18], [19] and considered likely to be functional. As shown in Table 1, rs2834167A/A genotype (47K/K) was significantly increased in SSc under the recessive model (P = 0.038, odds ratio [OR] = 1.61, 95% confidence interval [CI]: 1.02–2.54). The genotype frequency in our controls was compatible with Hardy–Weinberg equilibrium, and was quite similar to that in
Discussion
In the present study, we showed that rs2834167 coding for IL10RB E47K was associated with susceptibility to dcSSc. IL10RB gene has never been studied for the association of SSc. Our findings provided new evidence that supports the causal role of IL-10 or related cytokine signaling in the pathogenesis of SSc.
IL-10 stimulates B cells and T helper 2 (Th2) cells, which may result in production of autoantibodies. In the TSK/+ mouse, a genetic model for human SSc, loss of CD19 significantly decreased
Acknowledgments
This work was supported by Grant-in-Aid for Scientific Research on Priority Areas ‘Applied Genomics’ from the Ministry of Education, Culture, Sports, Science and Technology of Japan, Grant-in-Aid for Scientific Research (B) from Japan Society for the Promotion of Science (JSPS), grants from the Ministry of Health, Labour and Welfare of Japan, Japan Rheumatism Foundation and The Naito Foundation.
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