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العنوان
Immunopathogenesis of atopic dermatitis /
المؤلف
Mohamed, Shaymaa El Mongy.
هيئة الاعداد
باحث / شيماء المنجى المنجى محمد
مشرف / ساميه السعيد عبدالنبى
مشرف / فرحه عبد العزيز الشناوى
مشرف / فوزيه أمين سعفان
مشرف / حنان أحمد سالم
الموضوع
Skin diseaes-- Immunology.
تاريخ النشر
1997.
عدد الصفحات
271 p. :
اللغة
الإنجليزية
الدرجة
الدكتوراه
التخصص
الأمراض الجلدية
تاريخ الإجازة
1/1/1997
مكان الإجازة
جامعة المنصورة - كلية الطب - Department of Dermatology
الفهرس
Only 14 pages are availabe for public view

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from 297

Abstract

Atopic dermatitis is a chronic and relapsing inflammatory skin ease that often begins in infancy. It is characterized by typically istributed eczematoid skin lesions with lichenification and pruritic [excoriations. As in other atopic diseases a familial disposition and an [increasing incidence have been reported over the last few years. Diagnosis [of AD depends mainly on history, morphology and distribution of the [disease according to Hanifin and Rajka( 1980). To reach to the initiating I allergen is very important but not easy and can be reached by careful [history taking and prick test which can provide a confirmatory evidence to [suspected allergen. The skin lesions of AD are infiltrated by activated T-cells, I eosinophils and antigen-presenting Langerhans cells, that bind IgE on the I cell surface. This raises the possibility that a dysfunction of the IgE -I related cellular immune system may provide a link between the skin reaction to aeroallergens and the formation of skin lesions in AD. It was recently demonstrated by in situ hybridization that SIL associated with the allergen-induced late phase reaction express m RNA for IL-3, IL-4, IL-5 and GM-CSF. These data could be confirmed in AD patients by culturing allergen-specific T-cell clones from skin lesions showing a Th2 -related cytokine pattern with production of IL-4 and IL-5 but not IL-2 or IFNy. Immunologically it had been found that there is a defect in the suppressor T-cell (T8) population in AD patients which permits the formation of excess anaphylactic antibodies mainly IgE.