الفهرس 
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Abstract
Psoriasis is chronic, relapsing, immune- mediated inflammatory skin disease affecting 1-3% of the world population. Clinical manifestations of psoriasis are heterogeneous, ranges from limited to extensive disease. The majority of patients approximately 80% have limited disease while approximately 20% have extensive disease. The most characteristic lesion consists of red ,scaly sharply demarcated, erythematous plaques, present particularly over extensor surfaces ,and the scalp. The disease is variable in extent, duration and periodicity of flares. The etiology of psoriasis is unknown, but evolving evidence that it is a complex disorder caused by interaction of multiple factors include immunological, environmental and genetic factors . Histologically, psoriasis is characterized by marked keratinocyte hyperproliferation, a dense inflammatory infiltrate consisting of T cells and neutrophils, and vascular dilatation and proliferation. The primary defect in psoriasis patients was believed to be abnormal epidermal cells proliferation. The very early lesion of psoriasis is characterized by an inflammatory infiltrate of mononuclear cells in the upper dermis with only minimal changes in the epidermis. Thus, systemic effects of circulating cytokines may play an important role in the induction of epidermal cell proliferation. Psoriasis can be described as an autoimmune T-cell-mediated disease. Interaction between T lymphocytes and keratinocytes, via a variety of pro-inflammatory cytokines (IFN-γ, IL-12, TNF-α) and Summary 110 chemokines induce epidermal cell proliferation and play an important role in the pathogenic process of psoriasis . The aim of the current study was to assess the level of serum Interferon gamma in psoriatic patients and its relationship with the severity of the disease. Interferon gamma is a Th1-type, pro-inflammatory cytokine primarily secreted by T cells and natural killer cells, is involved in so many aspects of the immune response. Interferon- γ is considered a key cytokine in the pathogenesis of psoriasis , The suggested mechanisms are that interferon gamma is capable of inducing the expression of intercellular adhesion molecule 1 (ICAM-1) and HLA-DR, thus mediating interactions between inflammatory T cells and keratinocytes facilitating T cell migration to lesional epidermis,In addition to its action as anti-apoptotic factor for keratinocytes. To approach our goal this study was carried out on forty patients suffering from plaque, erythrodermic and guttate psoriasis and forty age and sex matched healthy volunteers and blood donors ,All of them were collected from the outpatient Clinic of the Dermatology Department, Faculty of medicine, Menofiya university in the period between April 2011 and April 2013.After taking a written consent, all cases were subjected to complete history taking, full general examination and detailed dermatological examination including assessment of PASI score. Venous blood samples (5–10mL) were taken under sterile conditions using the ELISA kit serum interferon gamma was measured.