Affiliations: [a] Skin Research Centre, Shahid Beheshti University of Medical Sciences, Tehran, Iran | [b] Biology Department, East Tehran Branch, Islamic Azad University, Tehran, Iran | [c] Autoimmune Bullous Diseases Research Center, Tehran University of Medical Sciences, Tehran, Iran | [d] Urogenital Stem Cell Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran | [e] Lübeck Institute of Experimental Dermatology, University of Lübeck, Lübeck, Germany | [f] Institute of Anatomy, University of Lübeck, Lübeck, Germany
Correspondence:
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Corresponding author: Reza Akbarzadeh, Institute of Anatomy, University of Lübeck, Ratzeburger Allee 160, D-23562 Lübeck, Germany. Tel.: +49 451 310 17152; Fax: +49 451 310 17104; E-mail: akbarzadeh@anat.uni-luebeck.de.
Note: [1] Equal contributors.
Abstract: BACKGROUND: TNF-α -308G/A polymorphism has been investigated in few studies for an association with susceptibility to bullous pemphigoid (BP) and alopecia areata (AA). Yet, these findings had so far not been independently replicated, and no data on a possible association of TNFα -308G/A polymorphism with these diseases in Iranian population were available. OBJECTIVES: In the present study, a possible effect of TNF-α -308G/A variation on susceptibility to BP or AA disease was evaluated. METHODS: Genomic DNA was extracted from the blood of the patients with BP and AA as well as control subjects which genotyped for the TNF-α -308 G/A polymorphism. TNF-α gene expression levels were analyzed by real-time RT-PCR. RESULTS: No association was observed between the TNF-α -308 G/A variation and susceptibility to BP or AA diseases in our Iranian cohort. In contrast to AA patients, expression of TNF-α gene was significantly higher in BP patients compared to control group. TNF-α gene was found to be similarly expressed in mutant and wild-type genotypes. CONCLUSIONS: TNF-α -308G/A polymorphism is not associated with the risk to develop of BP and AA in our Iranian cohort. Furthermore, this polymorphism is contributed to altering the levels of gene expression in BP disease.
