الفهرس 
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Abstract
SUMMARY
A
lopecia areata (AA) is a common non-scarring, patchy hair loss. Its exact pathogenesis is still uncertain but it is hypothesized to be an organ-specific autoimmune disease mediated by T lymphocytes directed to hair follicles. Genetic predisposition and environmental factors may trigger the initiation of the disease.
Osteopontin (OPN) is an acidic glycoprotein expressed by a variety of tissues and cell types, including immune cells. OPN is multifunctional and its functions are linked to various physiological and pathological events.
Osteopontin expression was described to be elevated in type-1 (cell mediated) diseases that affect the skin. There is evidence for a key role of OPN in Th1- and Th17 mediated diseases.
In our study we assessed the serum OPN in alopecia areata patients in comparison with that of controls, in an attempt to uncover the role of serum OPN in the pathogenesis of alopecia areata.
Fifty alopecia areata patients and fifty normal individuals were enrolled in the study, from which blood samples were drawn. Serum OPN was measured using ELISA test. The results showed significantly higher serum OPN in AA patients than that in the controls.
The assumed role of OPN in AA was based the fact that OPN exerts a Th 1 cytokine function and is defined as a regulator of inflammatory cell accumulation and function at the sites of inflammation and repair, and it has been linked to other autoimmune inflammatory disease like psoriasis which is a Th1 mediated disease. On the other hand, AA is characterized by increase in the immunologic activity of Th1 cells.
In addition, OPN is known to be expressed by inflammatory cells as macrophages, dendritic cells, natural killer cells, T cells and B cells.These cells have been detected in the perifollicular infiltrates of AA and proved to be involved in the pathogenesis of AA.
The possible role of OPN in the pathogenesis of AA was supported by the detection of significantly elevated serum OPN levels in patients than that in controls. Thus, supporting our assumption that OPN participates in the autoimmune response against the hair follicle in AA, verifying its role in the pathogenesis of the disease.