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Deletion of late cornified envelope genes,LCE3C_LCE3B-del,is not associated with psoriatic arthritis in Tunisian patients
Authors:Bouchlaka Souissi Chiraz  Ammar Myriam  Zarra Ines  Jordan Catherine  Bouazizi Fatma  Cheour Ilhem  Tekaya Raoudha  Zeglaoui Hela  Fourati Hela  Bouajina Elyes  Doss Nejib  Helms Cindy  Elgaaied Amel  Sellami Slaheddine
Institution:1. Laboratory of Genetics, Immunology and Human Pathologies, Faculty of Sciences, University of Tunis El Manar, 2092, Tunis, Tunisia
2. Dermatology Department, La Rabta Hospital, 1007, Tunis, Tunisia
3. Division of Human Genetics, Department of Genetics, Washington University School of Medicine, St. Louis, MO, 63110, USA
4. Osteoarthritis-osteoporosis Research Laboratory, Rheumatology Department, LaRabta Hospital, 1007, Tunis, Tunisia
5. Rheumatology Department, Charles Nicolle Hospital, 1006, Tunis, Tunisia
6. Rheumatology Department, Farhat Hached Hospital, 4000, Sousse, Tunisia
7. Rheumatology Department, Hedi Chaker Hospital, 3029, Sfax, Tunisia
8. Dermatology Department, Military Hospital, 1008, Tunis, Tunisia
Abstract:A deletion of two genes from the late cornified envelope (LCE), LCE3B and LCE3C within epidermal differentiation complex on chromosome 1 was shown to be associated with both psoriasis and psoriatic arthritis (PsA) in several populations. To assess whether this deletion may contribute to the genetic predisposition to PsA in Tunisia, a total of 73 patients with PsA and 120 healthy matched controls were screened for the deletion, LCE3C_LCE3B-del, and its tag SNP, rs4112788. We also evaluated a possible relationship between PSORS1 and LCE3C_LCE3B-del through genotyping two proxy markers to HLA-C (rs12191877 and rs2073048). Our results did not provide evidence for association between the LCE3C_LCE3B-del nor the rs4112788 and the PsA. Similarly, no significant epistatic effect was observed. Our data suggest that The LCE deletion, previously identified in patients with psoriasis, is not of a major importance in the development of PsA in Tunisian patients supporting the current perception that different genetic risk factors contribute to skin and joint disease. However, these results need to be confirmed by additional large-scale studies of Tunisian PsA patients and controls.
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