Psoriasis and melanogenesis: which differences between psoriatic and healthy skin?

Psoriasis is a common chronic inflammatory skin disease characterized by hyperproliferative epidermis and mixed cutaneous lymphocytic infiltrate that occurs in genetically predisposed individuals. Many immune-derived cytokines, including interleukin (IL)-1, IL-6, IL-17, IL-19, IL-20, IL-22, tumour necrosis factor (TNF)-a and interferon (IFN)s, are over-expressed in psoriasis skin which may contribute to psoriatic skin inflammation and can also regulate keratinocyte proliferation. It has been demonstrated that keratinocytes synthesize and secrete many cytokines; some of these interact with many other skin cells, particularly with melanocytes. Melanocytes produce melanin by melanogenesis complex biochemical pathway. Keratinocytes, melanocytes communicate with each other by secreted factors and by cell-cell contacts. Particularly, keratinocytes control melanocyte growth and activity through a system of paracrine growth factors and cell adhesion molecules. In addition, several keratinocyte-derived cytokines known to inhibit human melanogenesis have been identified; these include transforming growth factor-? (TGF-?), INF-?, IL-1, IL-6, TNF-?. The possible immunological interaction between psoriasis and melanogenesis is particularly interesting for clinical and therapeutic implications. Aim of our study was to investigate possible differences in melanogenesis markers between psoriatic and healthy skin. In particular, we analyzed the possible involvement of Tyrosinase, MITF, and BMP-4. Our study evidenced a reduction of Tyrosinase, MITF and BMP-4 in psoriatic skin respect to healthy skin.