Polymorphism of FAS and FAS ligand genes in alopecia areata: A case–control study in Egyptian population
Iman Seleit, Ola Ahmed Bakry, Eman Abd El Gayed and 1 more
Indian Journal of Dermatology · 2018
doi:10.4103/ijd.ijd_286_17 (opens in a new tab)
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Abstract
Background: Alopecia areata (AA) is a common dermatologic disease with suspected autoimmune etiology. Tumor necrosis factor superfamily member 6 or CD95 (FAS) and FAS ligand (FASL) are proapoptotic proteins. The relationship between apoptosis and autoimmunity is well recognized. Inflammatory T cells in AA are cytotoxic and possess FAS/FASL antigens. Aim: This study aims to investigate the association between FAS-670 A/G and FASL-124 A/G gene polymorphisms and AA to clarify if these polymorphisms influence disease occurrence or increase disease risk. Materials and Methods: A case–control study was conducted on sixty patients with AA, and 40 age- and sex-matched healthy subjects, as a control group. Disease severity was assessed by severity of alopecia tool (SALT) Score. FAS 670A/G and FASL 124A/G gene polymorphisms were investigated by the restriction fragment length polymorphism polymerase chain reaction. Results: For FAS gene, G/G genotype was significantly higher in cases than in control group with odds ratio 5.1. G allele was more prevalent among patient group with odds ratio 1.75. For FASL gene, A/G genotype was significantly higher in cases than in control group with odds ratio 4.53. G allele was more prevalent among patient group with odds ratio 1.88. GG genotype of FAS was significantly associated with longer disease duration (P=0.001), recurrent attacks (P=0.01), higher SALT score (P=0.009), alopecia universalis (P=0.002), and severe disease (P=0.006). Conclusion: FAS and FASL gene polymorphisms are associated with AA. Further large-scale studies on different ethnicities are required for more clarification of their role in disease development. Therapeutic modalities based on their inhibition could be promising in the treatment of a common disease like AA.
Abstract licence: CC BY-NC-SA
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