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""Epidermal growth factor receptors (EGFRs) are overexpressed in psoriatic keratinocytes, and regulate cell growth, proliferation and differentiation through binding to epidermal growth factor (EGF). The role of EGF and EGFRs in the pathogenesis of psoriasis and the contribution of their measurement to psoriasis management are still unknown. To evaluate serum concentrations of EGF, soluble (s)EGFRs and EGF content in psoriatic scales [http://www.selleckchem.com/products/3-methyladenine.html 3-MA purchase] of patients with severe psoriasis, and to analyse their association with the clinical activity of the disease. Serum samples and plaque scales were collected from 51 patients with plaque-type psoriasis. Concentrations of EGF and sEGFR in serum and of EGF in scales were measured using enzyme immunoassay. Data were analysed with respect to baseline Psoriasis Area and Severity Index (PASI). Mean serum EGF concentration in patients was higher [http://www.selleckchem.com/screening/chemical-library.html Compound Library] than in controls (701?��?72 vs. 586?��?63?pg/mL), but the difference was not significant. Mean serum concentration of sEGFR was significantly lower than controls (40.8?��?1.4 vs. 86.4?��?11.3?ng/mL, P??20, and this was significantly higher than the mean of 414?��?82?pg/mL in the group with PASI?[http://en.wikipedia.org/wiki/Resiquimod Resiquimod] seve""Genetic deficiency of type XVII collagen (C17), laminin-332 or type VII collagen causes epidermolysis bullosa (EB). Spontaneous correction of the deficiency, also known as revertant mosaicism, is caused by a second somatic mutation that restores protein expression resulting in clinically healthy (revertant) patches surrounded by fragile (mutant) skin. Interestingly, in some patients, patches of revertant skin show hyperpigmentation. To study the possible role of affected proteins in pigmentation and melanocyte distribution, we investigated clinical documentation and skin biopsy specimens of 13 revertant EB patients having correcting mutations in the COL17A1, LAMB3 or COL7A1 genes. Analysis revealed that lack of C17 led to decreased melanin intensity and melanocyte density in the epidermis when compared with the revertant patches. Reversions of LAMB3 and COL7A1 in keratinocytes did not influence clinical pigmentation or density of melanocytes. We conclude that in human skin, melanocyte supply to the epidermis depends on C17 expression in keratinocytes.