الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
Psoriasis, a chronic papulosquamous inflammatory skin disease, is one of the commonest immune-mediated disorders. The evolving evidence suggests that psoriasis is a complex disorder caused by the interaction of multiple genes, the immune system, and environmental factors. Psoriasis is characterized by scaly, erythematous lesions with sharply demarcated margins. Psoriasis generally involves differentiation of lesions based on: a. morphology of the lesions, b. degree of inflammation, c. distributing patterns of the lesions, d. extent of body surface involvement, e. first onset and f. velocity of propagation. Psoriasis is characterized by abnormalities of the papillary dermal vasculature. Micro vessels in the papillary dermis of psoriatic plaques are tortuous and dilated. Recently, Ang-1 and Ang-2 are identified as endogenous glycoprotein. Their binding to Tie -2 is important for angiogenesis process. Ang-1 and Ang-2 antagonize each other. In psoriasis, Ang–Tie-2 system is activated in papillary dermis. Ang-2 is capable of sensitizing endothelial cells to several inflammatory signals facilitating leucocytes adhesion and chemotaxis and contributing to inflammatory response during development of psoriasis. NB-UVB therapy reduces keratinocyte proliferation. The direct effect of NB-UVB is mostly restricted to the epidermis and upper part of papillary dermis. It reduces the numbers of LC and DCs, suppresses Th1 and Th17 signaling Therefore, this study planned to find out whether there is a relation between Ang-2 level and severity of disease and treatment with NB-UVB.