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العنوان
THE ROLE OF THE INTERLEUKIN
23R GENE POLYMORPHISM IN
PSORIASIS
الناشر
Mona Fathy Sayed Ahmed
المؤلف
Ahmed ,Mona Fathy Sayed
هيئة الاعداد
مشرف / Riham Assem El Essawy
مشرف / Azza Mohamed El Khawaga
مشرف / Ola Abd Almonem El Sisi
مشرف / Mona Fathy Sayed Ahmed
تاريخ النشر
2012
عدد الصفحات
118
اللغة
الإنجليزية
الدرجة
الدكتوراه
التخصص
الطب
تاريخ الإجازة
1/1/2012
مكان الإجازة
اتحاد مكتبات الجامعات المصرية - Clinical and Chemical Pathology
الفهرس
Only 14 pages are availabe for public view

from 118

from 118

Abstract

Psoriasis is a common inflammatory skin disease with a prevalence varying between 0.1 and 3% in different parts of the world. The most common form of psoriasis is plaque psoriasis. Patients may inherit a predisposition to psoriasis, although the disease is expressed only after being triggered by certain environmental or antigenic factors. Multiple independent genome-wide scans have been performed revealing a number of linked genetic loci, some of which achieve statistical significance. External and internal factors may provoke psoriasis in a genetically predisposed individual such as environmental factors, physical trauma, and psychological stress, several drugs, bacterial, viral, and yeast infections. IL-23/Th17 inflammatory pathway is critically involved in psoriasis pathogenesis. Receptors of IL-23 are a heterodimeric receptor composed of the IL-12 receptor β1 (IL-12Rβ1) and IL-23 receptor (IL-23R), Binding of IL23 activates Janus kinase 2 (Jak2), tyrosine kinase 2 (Tyk2), and signal transducers and activators of transcription (STATs) 1, 3, 4, and 5. The IL23R gene is located on the short (p) arm of chromosome 1. The gene coding for the other component of the receptor is IL12Rβ1 on chromosome 19p. There are different polymorphisms in the IL23R gene which may lead to protective effect, or they increase the incidence of certain disorders. Variations in the IL23R gene have also been associated with psoriasis. One of the most important polymorphisms in the IL-23R is at 381position termed rs11209026 This associated SNP, consisting in a guanine (G) to adenine (A) substitution at DNA level, results in an arginine (R) to glutamine (Q) substitution in position 381 (R381Q), rs11209026, also named as Arg381Gln. Change to glutamine arrests the IL-23R signaling cascade and prevents inflammatory responses induced by Th17 cells and protects from multiple immune-mediated diseases by impairing IL-23-mediated Th17 responses.
Our study was performed on 30 psoriatic patients and 30 healthy volunteers as controls. Real time PCR was used for studying the rs11209026 SNP, while PCR-RFLP analysis was used for the rs2201841SNP. We observed that G allele in rs11209026 SNP was risky compared to A allele (OR=6.510, CI=1.376-30.792) with significant difference in the distribution of the A&G alleles between the two studied groups (p-value=0.008). However, the rs2201841 A&G alleles were not significantly associated with psoriasis (p-value=0.211, OR=1.893, CI=0.689-5.200). in conclusion, IL23R Arg381Gln (rs11209026 ) has a strong protective effect may be through interfering with signaling of IL23 at its receptor site, targeting of this IL23R SNP may lead to dramatic clinical improvement in patients with psoriasis. We recommended for Studies based on larger population to clarify the role of rs2201841 and to confirm our findings.