Psoriasis is an autoimmune chronic skin disease with features, such as abnormal growth and differentiation of keratinocytes, increased vasodilation with local release of nitric oxide (NO), and skin infiltration by leukocytes. The most common form, psoriasis vulgaris, is characterized by erythematous plaques covered by thick white scales. Although psoriatic skin lesions are mostly found on the extensor surfaces of the body, any part of the body including the scalp and nails can develop a lesion. It is well established that psoriatic lesions are triggered by trauma, also known as Koebner phenomenon. Psoriasis and wound healing share common features. In both conditions, the expression of keratins I and X is reduced, while keratins VI and XVI are upregulated in comparison with the normal skin. Moreover, the psoriatic skin lesion expresses antimicrobial peptides as well as the antimicrobial protein REG3A that regulates keratinocyte proliferation and differentiation after skin injury. However, in psoriasis keratinocytes are not able to differentiate due to elevated intracellular Ca++concentration; this leads to keratinocyte hyperproliferation and subsequently increased rate of wound healing.