Polymorphisms in the ATG16L1 Gene are Associated with Psoriasis Vulgaris

Abstract

Psoriasis is an immune-mediated inflammatory disorder\nof the skin with a complex pathogenesis and a strong\ngenetic component (1). Several regions in the genome,\nincluding the psoriasis susceptibility locus 1 (PSOR1),\nhave been identified as conferring susceptibility to psoriasis\n(2–4). However, the complete genetic background\nof psoriasis remains to be established. Autophagy is a\nfundamental biological process that is involved in cell\ngrowth and plays a role in innate and adaptive immunity.\nIn particular, autophagy-selective responses contribute\nto inflammatory bowel disease (IBD) (5, 6), neurodegeneration\n(7), and cancer (8). The ATG16L1 protein,\nwhich is encoded by the ATG16L1 gene (2q37), is a key\ncomponent of a large protein complex essential for autophagy\n(9), and polymorphisms within this gene have\nbeen reported to be associated with Crohn’s disease (5).\nTaking into consideration that genes in the autophagy\npathway play an important role in inflammation and\nimmunity, and as a part of our ongoing research on the\nimpact of genetic variants to the risk of psoriasis vulgaris,\nthe aim of the present study was to assess whether\npolymorphisms in ATG16L1 gene might also contribute\nto the risk of psoriasis.