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Recent genome-wide association studies (GWASs) have identified &gt;20 new loci associated with the susceptibility to psoriasis vulgaris (PsV) risk. We investigated the association of PsV and its main clinical subphenotypes with 32 loci having previous genome-wide evidence of association with PsV ( P  &lt; 5e−8) or strong GWAS evidence ( P  &lt; 5e−5 in discovery and  P  &lt; 0.05 in replication sample) in a large cohort of PsV patients ( n  = 2005) and controls ( n  = 1497). We provide the first independent replication for  COG6  ( P  = 0.00079) and  SERPINB8  ( P  = 0.048) loci with PsV. In those patients having developed psoriatic arthritis ( n  = 955), we found, for the first time, a strong association with  IFIH1  ( P  = 0.013). Analyses of clinically relevant PsV subtypes yielded a significant association of severity of cutaneous disease with variation at  LCE3D  locus ( P  = 0.0005) in PsV and nail involvement with  IL1RN  in purely cutaneous psoriasis (PsC,  P  = 0.007). In an exploratory analysis of epistasis, we replicated the previously described  HLA-C–ERAP1  interaction with PsC. Our findings show that common genetic variants associated with a complex phenotype like PsV influence different subphenotypes of high clinical relevance.

Risk variants for psoriasis vulgaris in a large case–control collection and association with clinical subphenotypes