Reyhaneh Abgoon
Islamic Azad University, Iran
Title: Investigation of IL-12B gene polymorphism (rs3212227) in Iranian patients with alopecia areata
Biography
Biography: Reyhaneh Abgoon
Abstract
Objective: Alopecia areata (AA) is an autoimmune disease characterized by patchy hair loss aff ecting both scalp and body hair. Although the etiology and pathogenesis of this disease are still unknown, a polymorphism within IL-12B gene has been described in few studies to be associated with AA susceptibility. Yet, these fi ndings had so far not been independently replicated, and no data on a possible association of IL-12B mutation and AA in Iranian population were available.
Methods: Th is study contains 30 AA patients and 15 healthy controls. Genomic DNA was isolated using DNG-plus and PCRRFLP analysis was performed to detect IL-12B rs3212227 polymorphism. Several relevant information such as demographic data (age, gender) or clinical characteristics were analyzed for a possible eff ect of these factors on susceptibility to AA in patients who carry CC, AC, and AA genotypes.
Results: No association between the IL-12B rs3212227 mutation and susceptibility to AA was observed in our Iranian cohort. PCR-RFLP results showed that frequency of CC genotype (13.3% vs. 6.6%) are similar in both patient and control groups. AC genotype was detected in 46.6% and 6.6% of patients and controls, respectively. Th e AA genotype which is wild genotype had a higher frequency in healthy individuals. Statistical analyses indicate that there is no signifi cant diff erence in the distribution of genotypes between patients and controls (P=0.12). Although the C allele frequency of IL-12B was higher in the patients than control subjects (36.6% vs. 10% respectively), but there is no signifi cant diff erence (P=0.12).
Conclusion: We here demonstrate that the IL-12B rs3212227 polymorphism is not associated with the risk to develop AA in our Iranian cohort. Th erefore, this study failed to confi rm a reported association between gene mutation and susceptibility to AA. Hence, the genetic predisposition to develop AA greatly varies among diff erent ethnic groups.