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Updated: Jan 2, 2026

Candidate Gene Testing in Clinical Cohort Studies with Multiplexed Genotyping and Mass Spectrometry
Published on: June 21, 2018
Genetic variants within ANRIL (antisense non coding RNA in the INK4 locus) are associated with risk of psoriasis
Azadeh Rakhshan1, Nader Zarrinpour2, Afshin Moradi3
1Department of Pathology, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Background:
Psoriasis 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.
Methods:
We 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.
Results:
The 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).
Conclusion:
Consequently, 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.
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