Psoriasis (MIM 177900) is a chronic immune-mediated and hyperproliferative disorder of the skin that affects up to 3% of the Caucasian population. Psoriasis is a non-infectious disease and in addition to the skin, nails and joints can also be affected. The signs and symptoms of psoriasis usually appear between the ages of 15 and 35. About 75% of patients develop psoriasis before age 40. However, it is possible to develop it at any age and there is another peak onset period between the ages of 50 and 60. About 80% of people with psoriasis have plaque psoriasis which appears as patches of raised, reddish skin covered by silvery-white scale. About 15% of people who develop psoriasis get a related form of arthritis called psoriatic arthritis which causes inflammation of the joints.
The disease has a strong genetic compound as evidenced by high sibling risk ratio λS of 4-11. Besides the familial accumulation and the high concordance in monozygotic twin-pairs (~70% versus 20% in dizygotic twins) there is a strong association with the MHC class I region (PSORS1: psoriasis susceptibility locus 1) that was already demonstrated in the 1970s. In several studies, polymorphisms in IL12B and IL23R have been found to be associated with psoriasis susceptibility. Other loci with newly confirmed association encode IL23A, a protein involved in IL-23 signaling, TNIP1 and TNFAIP3, two proteins that regulate NF-кB signaling, and IL4 and IL13 that are involved in the modulation of Th2 immune responses.
Because psoriasis has such a strong genetic background, it is our goal to characterize the genetic causes of disease pathogenesis, as a prerequisite for a customized therapy for this distressing disease.