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Psoriasis is an immune-mediated inflammatory disorder of the skin with a complex pathogenesis and a strong genetic component (1). Several regions in the genome, including the psoriasis susceptibility locus 1 (PSORl), have been identified as conferring susceptibility to psoriasis (2—4). However, the complete genetic background of psoriasis remains to be established. Autophagy is a fundamental biological process that is involved in cell growth and plays a role in innate and adaptive immunity. In particular, autophagy-selective responses contribute to inflammatory bowel disease (IBD) (5, 6), neurodegeneration (7), and cancer (8). The ATG16L1 protein, which is encoded by the ATG16L1 gene (2q37), is a key component of a large protein complex essential for autophagy (9), and polymorphisms within this gene have been reported to be associated with Crohn's disease (5). Taking into consideration that genes in the autophagy pathway play an important role in inflammation and immunity, and as a part of our ongoing research on the impact of genetic variants to the risk of psoriasis vulgaris, the aim of the present study was to assess whether polymorphisms in ATG16L1 gene might also contribute to the risk of psoriasis.

Polymorphisms in the ATG16L1 Gene are Associated with Psoriasis Vulgaris