Psoriasis is a chronic, inflammatory, hyperproliferative disease of the skin, scalp, nails, and joints, with a prevalence of up to 2% in Caucasians^1,2 but well under 1% in the Mongoloid races of the Far East.³ The disease varies in severity. Some patients display mild disease with isolated scaling erythematous plaques on the elbows or knees, whereas for others most of their cutaneous surface can be affected. At the cellular level, psoriasis is characterised by markedly increased epidermal proliferation and incomplete differentiation, elongation, dilation, and leakiness of the superficial plexus of dermal capillaries, and by a mixed inflammatory and immune cell infiltrate of the epidermis and papillary dermis.^1,2 Dermal infiltrates comprised of T cells and macrophages typically appear in early lesions before epidermal changes.⁴ The therapeutic effect of immunosuppressive agents suggests psoriasis has a primary immune pathogenic basis.⁵

Susceptibility to the development of psoriasis is likely to have a significant genetic component. Accumulating evidence is consistent with the idea that psoriasis is a multifactorial disorder caused by the concerted action of multiple disease genes in a single individual and triggered by environmental factors.⁶ Some of these genes control the severity of a variety of diseases, via their regulation of the inflammatory and immune processes (severity genes), whereas others are unique to psoriasis (specific genes).

A number of genetic studies have sought to identify the psoriasis susceptibility loci. Associations between psoriasis and human lymphocyte antigen alleles were first described in 1990.⁷ Subsequently, genome-wide linkage scans have mapped psoriasis to several chromosomal regions including PSORS1 at 6p21,^8,9 PSORS2 at 17q,^8–10 PSORS3 at 4q,¹¹ PSORS4 at 1q,¹² PSORS5 at 3q,¹³ PSORS6 at 19p,¹⁴ and PSORS7 at 1p.¹⁵ Recently, the International Psoriasis Genetics Consortium reassessed these candidate …