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العنوان
Evaluation of apoptosis-related gene FAS
and FASL polymorphisms in
alopecia areata /
المؤلف
Etifa, Doaa Mohammed Abd Elgawad.
هيئة الاعداد
باحث / دعاء محمذ عبذالجواد عطيفة
مشرف / إيمان عبد الفتاح سليط
مشرف / علاء أحمد بكرى
الموضوع
Alopecia areata. Hair - Care and hygiene. Baldness - Alternative treatment.
تاريخ النشر
2017.
عدد الصفحات
171 p. :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
الأمراض الجلدية
الناشر
تاريخ الإجازة
10/9/2017
مكان الإجازة
جامعة المنوفية - كلية الطب - الأمرض الجلدية والتناسلية وأمراض الزكورة
الفهرس
Only 14 pages are availabe for public view

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Abstract

Alopecia areata is a disfiguring disease characterized by
nonscarring hair loss on the scalp or other parts of the body. It is
characterized by sudden loss of hair in rounded or oval shaped single
or multiple patches with spontaneous remission, relapse, and
exacerbation. AA can develop into more severe forms; AT which
involves loss of all scalp hair and AU which means complete loss of
all body hair. Most evidence suppports the hypothesis that AA is a Tcell
mediated autoimmune disease of the hair follicles.
Alopecia areata has a multifactorial etiology so that several
genes and environmental factors come together with a different weight
in triggering the pathology. Moreover, AA clusters in families; 10 25
% of all patients have affected relatives.
Apoptosis is an essential process in immune homeostasis and
regulation, and it is particularly important in the termination of
immune responses. Defects in the elimination of cells or in the
processes can contribute to the breakdown of tolerance and
development of autoimmunity.
FAS and FASL are important proapoptotic proteins, which
belong to the tumor necrosis factor superfamily and play essential
roles in many human autoimmune diseases.
The human FAS gene is located on chromosome 10q24.1 while
the human FASL gene is located on chromosome 1q23.
A to G substitution at position 670 in the promoter region of
FAS may destroy the binding elements for stimulatory protein 1(Sp1)
and signal transducer and activator of transcription protein 1 (STAT1),
thus leading to decreased promoter activity and FAS expression.