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. 2018 Mar 14;8:4529. doi: 10.1038/s41598-018-22574-5

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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HLA risk imparts a genetic association with age of disease onset. (A) The genetic risk score (GRS) was significantly and inversely correlated with age at diagnosis (linear regression analysis and Pearson correlation coefficient, P < 0.001, r = −0.227). (B) GRS was significantly different in patients when grouped into under 8, 8–16, and over 16 years old at diagnosis (Kruskal-Wallis ANOVA with Dunn’s posttest **P < 0.01, ****P < 0.0001). (C, D) The HLA-only GRS imparted a similar association with age at diagnosis as the full score (C: linear regression analysis and Pearson correlation coefficient, P < 0.001, r = −0.245; D: Kruskal-Wallis ANOVA with Dunn’s posttest *** P < 0.001, ****P < 0.0001). (E, F) The non-HLA GRS did not correlate with age at diagnosis (E: linear regression analysis and Pearson correlation coefficient, P > 0.05, r = −0.010; F: Kruskal-Wallis ANOVA with Dunn’s posttest P > 0.05). The 99% probability bands for linear regressions are depicted as dotted lines.