الفهرس 
abstractOnly 14 pages are availabe for public view
 |  | from | 111 |  |  |
| | | from | 111 | | |
Abstract
Psoriasis is a chronic, relapsing inflammatory disease potentially affecting all areas of the skin, nails, and mucous membranes that results from an interaction between an individual’s genetic susceptibility and specific environmental factors.
Th17 cells are present in the inflammatory infiltrate in psoriatic plaques to induce enhancement of neutrophil chemotaxis .
An initiating event such as trauma or skin surface microbes triggers IL-23 production by keratinocytes and resident dendritic cells, which in turn stimulates proliferation of CCR4+ and CCR6+Th17 cells found within skin. These activated Th17 cells secrete Th17 cytokines including IL-22 and IL-17A, which cause keratinocyte growth and activation, respectively.
Apart from IL-17(A), five additional IL- 17 members have been described (termed IL-17B to IL-17F), which all have conservations in their C-terminal region and also form homodimers.
IL-17 is an important mediator in tissue inflammation as it mobilizes neutrophils and induce the production of various cytokines and chemokines.
IL-17 has been reported to modulate the cytokine production and surface molecular make-up of epidermal keratinocytes. IL-17 enhanced the production of IL-6 and IL-8 in keratinocytes and induced a weak expression of ICAM-1 and HLA-DR [1]. TNFα- was markedly inhibited by IL-17. In addition, IL-17 has been reported to modulate fibroblast function by inducing their IL-6, IL-8, IL-11, GROα and G-CSF production.
The IL-23/IL-17 axis has been reported to be involved in immunity to several bacteria and the protective response against fungus and yeast infections and in autoimmune diseases.
This study was designed to detect the serum level of IL-17 in thirty chronic plaque psoriasis patients as compared to sex and age matched control subjects similar results had been obtained by earlier investigators.
In our study serum levels of this cytokine were significantly elevated and significantly correlated to PASI score, approving that Th17 and its cytokine might have essential role in psoriasis pathogenesis. This was in agreement with earlier results that detected a decrease in serum IL-17 after topical therapy.
There was statistically insignificant change in PASI and disease severity among patients on day 21 at the end of topical corticosteroid therapy. This could have been attributed to several factors .The short duration (21 days) of topical therapy might have been as a factor. However, the final and detailed results of these clinical trials are yet to be published.
.