الفهرس 
VitiligoOnly 14 pages are availabe for public view
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Abstract
Vitiligo is an acquired pigmentary disorder due to loss or destruction of melanocytes from the epidermis. The question about the presence of residual melanocytes in the depigmented skin remains unanswered.
There are three major hypotheses for the pathogenesis of vitiligo; biochemical/ cytotoxic, neural and autoimmune. Some data provide strong evidence supporting an autoimmune pathogenesis of vitiligo.
Defective adhesion seems to be involved in the chronic loss of melanocytes observed in vitiligo. Findings showed an association of genetic variants of an adhesion gene with vitiligo and reduced immunohistochemical expression of some adhesion molecules in vitiligo skin.
Plakoglobin (also known as γ-catenin) is a member of the Armadillo family of proteins and a structural and functional homolog of β-catenin. Catenin proteins have two major roles in the cell: the mediation of cell-cell adhesion and cell signaling. As adhesive proteins, both β-catenin and plakoglobin interact with the cytoplasmic domain of cadherins, thereby tethering the cadherin proteins to the cytoskeleton. In addition to their cell-cell adhesive functions, both β-catenin and plakoglobin interact with a number of intracellular partners including signaling proteins and transcription factors, which accounts for their involvement in cellular signaling.
The aim of the current study was to investigate the role of plakoglobin and β-catenin in vitiligo pathogenesis by immunohistochemical study of their expression in skin biopsies of this disease entity.
To elucidate this aim, 38 subjects were included in the study and divided in to two groups: (group1); included 18 patients with different clinical varieties of non-segmental vitiligo and (group 2); included 20 age and gender matched normal subjects as a control group.