Current research in pathogenesis of psoriasis vulgaris suggests that the inflammatory mechanisms are immune based and most likely initiated and maintained by T cells. However, the question of lymphocyte being an initiator of psoriatic events remains open so far. Clinical observations such as plaque symmetry, stress-induced onset or exacerbations, pruritus, and possibility of generalization, suggest a role of the nervous system and neurogenic inflammation in pathogenesis. A key to understanding the role of melanocyte in psoriasis is their ability to act as regulatory cell in maintaining epidermal homeostasis. In suggested hypothetic event, melanocyte, acting as a local "stress sensor", provide communicatory link between CNS and skin. The disease probably begins with so far unknown signal directed through neuronal network to the melanocyte, placed in the center of epidermal unit. That signal governs keratinocyte cellular activities and lead to reactive abnormal epidermal differentiation and hyperproliferation. Increased proliferation of basal keratinocytes and high metabolic demands creates angiogenesis in papillary dermis and elongation of dermal papillae. Stimulated melanocytes and basal keratinocytes become an important source of proinflammatory cytokines that attract lymphocytes in dermis. In conclusion, according to our hypothesis, lymphocyte infiltrate in psoriasis is secondary event rather than vice versa as presented in the literature.