الفهرس 
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Abstract
Atopic dermatitis is a multifactorial, chronic, relapsing, inflammatory skin disease. It is one of the most common skin disorders in children. Skin lesions are highly pruritic and eczematous, which have specific morphology and flexural distribution. It comprises itchy papules (occasionally vesicles in infants), which become excoriated and lichenified. The eruption is frequently associated with other atopic conditions in the same individual or other family members such as bronchial asthma, allergic rhinitis, and allergic conjunctivitis.
The clinical phenotype that characterizes AD is a product of complex interactions among genetically determined immune abnormalities that are influenced by environmental factors, the skin barrier defect, susceptibility to infection and immunological factors. AD is a skin allergic disease that is characterized by peripheral eosinophilia, mast cell activation and predominance of Th2 cells.
Galectin-9 is a member of the tandem-repeat galectin family, which is widely distributed in human tissues including epithelial tissues. Gal-9 binds to various partners expressed on the cell surface, such as T-cell Ig and TIM-3, CD44 and IgE. It has been well characterized as an eosinophilic chemoattractant. It also alters the T-cell balance by negatively regulating T-helper Th1 and Th17 cells, resulting in Th2 polarization. Gal-9 plays a variety of cellular roles, including modulation of cell differentiation, adhesion, aggregation and cell death. Through these functions gal-9 can regulate multiple physiological and pathological processes including allergy.
E selectin is expressed on the surface of activated endothelial cell upon stimulation by inflammatory cytokines. It enables adhesion of neutrophils, leukocytes and monocytes on activated endothelium in the skin. E selectin is found to be important in the pathogenesis of AD.
The aim of this study was to shed light on the role of galectin 9 and E selectin in AD pathogenesis through evaluation of their immunohistochemical expressions in involved skin in atopic dermatitis patients, in addition to correlate their evaluated expressions with the studied clinicopathological parameters of AD cases.
The study was carried out on 22 atopic dermatitis patients and 10 age and sex matched controls. They were subjected to full history taking, clinical examination. SCORAD score calculation was done for AD patients in the first visit. In addition, sections from lesional skin biopsies of atopic dermatitis cases, and from site matched of controls were stained with gal-9 and E selectin immunohistochemical stains.
The results of the current study showed that:
1- Atopic dermatitis patients exhibited a significant increased gal-9 H score, percent of expression, cellular localization (P˂0.00) and intensity (P=0.04) than controls in epidermal keratinocytes.
2- Galectin 9 expression in dermal cellular infiltrate was significantly higher in atopic dermatitis cases than controls (P ˂0.001).
3- There was a significant positive correlation between galectin 9 H score and SCORAD score of atopic dermatitis (P<0.001).
4- There was a significant elevation in H score of E selectin immunoreactivity (P=0.002) and its percent of expression (P=0.001) and cellular localization (P<0.001) in atopic dermatitis cases than controls in epidermal keratinocytes.
5- E selectin expression in dermal cellular infiltrate was significantly higher in atopic dermatitis cases than controls (81% versus 0) (P ˂0.001).
6- There was a non significant correlation between gal-9 H score and E selectin H score in atopic dermatitis patients (r=-0.03, P=0.86).