New immune system genetic polymorphisms associated with moderate-to-severe plaque psoriasis: a case-control study

R.P.P. and G.S.L. contributed equally to this manuscript. Dear Editor, Genes for factors such as interleukin‐23 receptor (IL‐23R), IL‐12B and tumour necrosis factor (TNF)‐α have been widely associated with psoriasis and related diseases [rheumatoid arthritis (RA), psoriatic arthritis (PsA) and Crohn disease (CD)].1 These genes are therapeutic targets to treat psoriasis. However, results with other candidate genes are controversial. Therefore, large‐scale studies are needed to verify the genetic factors that trigger psoriasis. We evaluated the possible association between 192 single‐nucleotide polymorphisms (SNPs) and moderate‐to‐severe chronic plaque psoriasis. This approach may help us to find new targets for safer and more effective drugs. We recruited 197 healthy volunteers without a personal or family history of psoriasis, and 198 patients with moderate‐to‐severe plaque psoriasis between 16 October 2007 and 17 December 2012, in four hospitals in Madrid, Spain. All patients were white. The protocol fulfilled Spanish law on biomedical research. DNA was obtained from peripheral blood samples (MagNA Pure® System; Roche, Pleasanton, CA, U.S.A.). All samples were sent to the Human Genotyping Unit (CEGEN, Madrid, Spain), except two samples that had insufficient volume, to genotype 192 SNPs (VeraCode genotyping platform; Illumina, San Diego, CA, U.S.A.). The SNPs were preselected based on reports of psoriasis and other autoimmune diseases (RA, PsA and CD; 449 articles). We finally selected SNPs based on minor allele frequency ≥ 0·05, and on the results of studies performed in white patients with psoriasis (Table S1; see Supporting Information).