الفهرس 
An overview of psoriasisOnly 14 pages are availabe for public view
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Abstract
Psoriasis is a common chronic condition characterized by thick scaling red plaques which can be either localized or widespread. The disorder is characterized by spontaneous remission and exacerbations. Over the years, psoriasis occupied the position of one of the most prevalent autoimmune diseases worldwide; it affects approximately 2-3% of the population. This fact along with its great burden –emotionally and physically- on patients made it the focus of a lot of researches and investigations. The exact pathogenesis of psoriasis is still a matter that changes every day with new theories and explanations.
For a long time psoriasis was believed to be a primary keratinocytes hyperproliferation disorder. Recent progress in the understanding of psoriasis has attributed its pathogenesis to the important role of T cells; specifically Th1 and Tc1-although it cannot be merely explained by T cell role only as mentioned above.
In psoriasis, the initial activation of T-lymphocytes requires three steps: binding, signal 1 and signal 2. Binding occurs between surface adhesion molecules of both T-lymphocytes and APCs, then additional interactions occur at “signal 1” between TCR on T-cell and MHC I or II on APC, a process that is followed by additional interactions “signal 2” which, in their absence, T-cells undergo anergy or apoptosis. The trafficking of T-cells into the skin involves three steps: rolling, binding and diapedesis. Activated T-cells produce Th-1 cytokines (IL-2, TNF-α, IFN-γ) which, along with chemokines and growth factors, are responsible for the inflammatory infiltrate, vascular changes and the epidermal hyperproliferation present in psoriasis.
Over the years Macrophage migration inhibitory factor was investigated and re-evaluated over and over again, initially MIF was identified as a lymphokine that plays an important role in cell-mediated immunity by concentrating macrophages at inflammatory loci, as well as by activating macrophages. Further studies revealed that MIF is secreted from many cells –immune and non immune-. Later on MIF was re-evaluated as a pro-inflammatory cytokine that is involved in a lot of inflammatory, autoimmune and even malignant diseases. Recently MIF was found to be a hormone that is secreted from pituitary gland itself in response to stressful events. This led Bucala, (2007) to describe it as the ”Most Interesting Factor”, a name that it truly deserves.
MIF was found to stimulate secretion of TNF-α as well as being stimulated by it. A positive inflammatory loop between both of them could explain the elevated level of MIF in psoriasis as well as its role in inducing the chronic inflammatory state of the disease. Moreover MIF inhibit P53 gene expression leading to inhibition of apoptosis this could explain the finding of kerationcytes hyperproliferation with administration of MIF.
The source of elevated MIF in psoriasis could be the T-cells, the keratinocytes, or other inflammatory cells. The exact role of MIF in psoriasis pathogenesis could be a primary role, or it may play a role in the evolution of psoriatic lesions but not a major or primary one and that more important factors (e.g.: TNF-α) may have the upper hand.
The present study was performed on 35psoriatic patients with different degrees of severity according to PASI score(28 mild, 6 moderate and one severe) of both sexes (19 males (54.3%) and 16 females (45.7%)], with the age ranging from 12 to 70 years old [mean ± SD: 35 ± 14 years) who had not received any systemic treatment for at least 4 months or local treatments for at least 2 months prior to the study. Serum MIF levels were measured by ELISA technique.