Funding sources This work was funded by grants from the Project of Shandong Provincial Clinical Medical Center for Dermatovenereology (2011), the Research Project of Shandong Provincial Science and Technology (2006GG2202060), the Project of Taishan scholar (2008) and the Project of Medical leading scholar of Shandong Province (2010).
Investigation of 20 non-HLA (human leucocyte antigen) psoriasis susceptibility loci in Chinese patients with psoriatic arthritis and psoriasis vulgaris
Article first published online: 25 APR 2013
© 2012 The Authors. BJD © 2012 British Association of Dermatologists
British Journal of Dermatology
Volume 168, Issue 5, pages 1060–1065, May 2013
How to Cite
Yang, Q., Liu, H., Qu, L., Fu, X., Yu, Y., Yu, G., Tian, H., Yu, Y., Sun, D., Peng, J., Bao, F., Yuan, C., Lu, N., Li, J., Zhang, Y. and Zhang, F. (2013), Investigation of 20 non-HLA (human leucocyte antigen) psoriasis susceptibility loci in Chinese patients with psoriatic arthritis and psoriasis vulgaris. British Journal of Dermatology, 168: 1060–1065. doi: 10.1111/bjd.12142
Conflicts of interest None declared.
Q.Y., H.L. and L.Q. contributed equally to this work.
- Issue published online: 25 APR 2013
- Article first published online: 25 APR 2013
- Accepted manuscript online: 18 DEC 2012 11:31AM EST
- Accepted for publication 10 November 2012
Background Recently, a number of non-HLA (human leucocyte antigen) psoriasis genetic susceptibility loci have been identified through genome-wide association studies, but data on their association with psoriatic arthritis (PsA) are lacking.
Objectives To investigate recently identified psoriasis susceptibility loci in a cohort of Chinese patients with PsA, psoriasis vulgaris (PsV) and healthy controls.
Methods Twenty single-nucleotide polymorphisms (SNPs) from 20 loci were selected for genotyping in 379 patients with PsA, 595 patients with PsV and 1181 healthy controls using the MassARRAY platform (Sequenom, San Diego, CA, U.S.A.). Data handling, quality control and association were performed using PLINK software, v. 1.07. The Cochran–Armitage trend test was used to test the genotype–phenotype association.
Results PsA showed a significant association with markers at TNIP1 (rs17728338, P = 2·20 × 10−8), IL28RA (rs4649203, P = 5·04 × 10−6), IL12B (rs2082412, P = 3·82 × 10−5), ERAP1 (rs27524, P = 1·25 × 10−3), PTTG1 (rs2431697, P = 1·22 × 10−3) and GJB2 (rs3751385, P = 1·48 × 10−3) when compared with the control group. In PsV a significant association was found for IL28RA (rs4649203, P = 9·53 × 10−7), TNIP1 (rs17728338, P = 1·21 × 10−4) and ERAP1 (rs27524, P = 1·17 × 10−3). The allele frequencies were not statistically different between PsA and PsV except for SNPs at IL12B and ZNF816A with a nominal P-value of 0·04 and 0·01, respectively.
Conclusions This study provides evidence for the involvement of ERAP1, IL28RA, GJB2 and PTTG1 loci in PsA susceptibility and confirmed the previously reported association with PsA and PsV. These results support the hypothesis that genetic aetiology of psoriasis is the same in both PsA and PsV and also support the higher genetic component of PsA than PsV.