الفهرس يوجد فقط 14 صفحة متاحة للعرض العام
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المستخلص
Psoriasis is an immunologically mediated, probably autoimmune disease in which T helper type 1 cytokine play an important role and it is characterized by hyperplasia and altered differentiation of epidermal keratinocytes. The etiology of psoriasis is unknown. It is associated with a strong genetic predisposition and various environmental and/or life style factors seem to be involved in the onset and/or exacerbation of psoriasis such as: infections, psychological factors, metabolic factors, trauma and drugs.
Psoriasis is recognized as a disease requiring the presence of activated T lymphocytes for its induction, expression and maintenance. There is growing evidence that activated T cells are the primary modulators in the pathogenesis of psoriasis. This is further supported by the fact that increased levels of activated T lymphocytes are present in psoriatic skin plaques and blood of patients especially elevated levels of activated CD4+ T helper lymphocytes were seen in both peripheral blood and lesional tissue. In addition, there is an increased number of effector T-cell subsets that have been shown in the epidermis and dermis of psoriatic plaques. Effector elements include skin homing CD4+ T helper cells and intraepidermal CD8+ T cell alter epidermal keratinocyte growth and drive the disease process.