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Abstract Psoriasis is a chronic, immune-mediated, recurrent disease of variable severity. It occurs more frequently in certain racial groups and geographical areas, possibly due to genetic and environmental factors. Psoriasis is defined as a long-lasting multifactorial inflammatory autoimmune skin condition precisely characterized by delimited, erythematic papules with adherent shiny scales. It has significant impacts on both physical and emotional health related quality of life comparable to other major illnesses. It is well known that CHI3L1 plays an important role in inflammation, proliferation and angiogenesis. In addition, CHI3L1 was found to play a role in the up-regulation of VEGF expression and enhanced angiogenesis. Thus, both CHI3L1 and VEGF may synergistically promote endothelial cell angiogenesis so it may play a role in the pathogenesis of psoriasis. The underlying principle behind (NB-UVB) treatment is that First, UV light induces apoptosis of keratinocytes and T cells in the epidermis and dermis. Second, UV light promotes immunosuppression by promoting migration of Langerhans cells (histiocytes) out of the epidermis. Lastly, UV light induces alterations in the cytokine profile of psoriasis, it shifts cytokine production in the direction of the counter-regulatory T helper 2 (Th2) immune response both locally and systemically. Thus play an important role in treatment of psoriasis. |