BackgroundPsoriasis is a systemic inflammatory disease which mostly affects skin. Evidences support the role of autoimmune responses in this disorder. The long non-coding RNA (lncRNA) antisense non coding RNA in the INK4 locus (ANRIL) has been shown to participate in modulation of immune response and in the pathogenesis of immune-related disorders. MethodsWe genotyped four single nucleotide polymorphisms (SNPs) with this lncRNA (rs1333045, rs1333048, rs4977574 and rs10757278) in 286 patients with psoriasis and 300 age-/sex-matched controls to identify the role of ANRIL as a risk locus for psoriasis. ResultsThe C allele of rs1333048 SNP was significantly more prevalent among cases compared with controls (OR (95% CI) = 1.56 (1.23–1.97), adjusted P value = 8.31E−4). The A allele of the rs4977574 had a protective effect against psoriasis (OR (95% CI) = 0.63 (0.49–0.81), adjusted P value = 0.001). The G allele of the rs10757278 conferred risk of psoriasis in the assessed population (OR (95% CI) = 1.9 (1.51–2.4), adjusted P value = 2.18 E−7). The C A G A haplotype (rs1333045, rs1333048, rs4977574 and rs10757278, respectively) was reported to be a protective haplotype against psoriasis (OR (95% CI) = 0.5 (0.35–0.71), adjusted P value = 0.001). The C A G G and T C G G haplotypes conferred risk of psoriasis in the assessed population (OR (95% CI) = 2.37 (1.59–3.54), adjusted P value = 2.4E−4; OR (95% CI) = 5.42 (2.88–10.22), adjusted P value = 1.1E−7, respectively). ConclusionConsequently, ANRIL can be regarded as a risk locus of psoriasis in the assessed population. Future studies are needed to verify whether this contribution is exerted through modulation of immune responses.