الفهرس 
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Abstract
Alopecia areata (AA) is a common form of localized, non-scarring hair loss. It is characterized by the loss of hair in patches, total loss of scalp hair (alopecia totalis), or total loss of body hair (alopecia universalis). Although there are several hypotheses proposed the etiology of alopecia areata, many factors have been described such as genetic susceptibility, the atopic state, nonspecific autoimmune reactions, neurological factors, infectious agents and possible emotional stress.
Interleukin 17 is a pro-inflammatory cytokine produced by T-helper cells and is induced by IL-23. In addition to its protective roles in host defense against microorganisms, the IL-17 pathway is implicated in the development of a variety of autoimmune diseases, such as rheumatoid arthritis, asthma, inflammatory bowel disease, and psoriasis. A large number of preclinical models have demonstrated important roles for IL-17 in the pathogenesis of several autoimmune diseases.
IL-17 appears to be involved in the autoimmune inflammation in AA and may provide CD4+-derived help to the CD8+ cytotoxic cells primarily involved in this disease. Previous data on IL17 gene polymorphisms in patients with alopecia areata are limited and the results are controversial. Therefor the aim of this work was to assess level of IL17 gene polymorphisms in patients of alopecia areata in comparison to healthy subjects in an attempt to assess its role in the pathogenesis of the disease. This study included 60 patients with alopecia areata and 40 age and gender matched normal subjects who served as controls. All patients were subjected to history taking and clinical evaluation to assess the clinical type of alopecia areata and its severity (SALT score).
Serum samples of 2 ml of venous blood were withdrawn from every case and control subject by sterile vein-puncture and transferred into an EDTA tube for DNA extraction and PCR.
DNA was extracted from whole blood using Qiagen Genomic DNA purification kit from USA. DNA was eluted stored at -200 C for further PCR procedure.
The results revealed that IL17 (G197A) Polymorphism (AA) genotype was significantly associated with alopecia areata patients (P = 0.001). It was present in 50% of cases compared with only 25% of healthy controls. Polymorphism (AA) genotype increase risk of occurrence of alopecia areata by 6.00 folds. (A) Allele was significantly associated with patient group (P = 0.001). It was present in 65% of cases compared with only 35% of healthy controls. (A) Allele increase risk of occurrence of alopecia areata by 3.65 folds. When patients with alopecia areata were compared in the current study according to clinical data a significant association was found between the IL17 (AA) genotype and non-patched AA (70%), progressive course (83%), severe disease (70%) and presence of nail changes (60%). There was a significant association between IL17 (A) allele and patchy alopecia areata (56%), progressive course (70%), severe disease (44%) and absence of nail changes (56%).
These results suggest that (AA) genotype and (A) Allele of IL17 (G197A) may be involved in the aetiopathogenesis of alopecia areata and may be associated with an increased predisposition to the disease. This role was suggested to be through the effect of IL17A polymorphism on IL-17 secretion as IL17A (G197A) is associated with increased IL-17 secretion. IL-17A is known to induce the expression of T-cell and dendritic cell chemokines, which lead to the migration of memory T cells and dendritic cells to the area of inflammation.