Involvement of the IL23/Th17 Pathway in the Pathogenesis of Tunisian Pemphigus Foliaceus. (12th July 2018)

• Record Type: Journal Article
• Authors: Ben Jmaa, M.; Abida, O.; Fakhfakh, R.; Bahloul, E.; Sellami, Kh.; Gaddour, L.; Elloumi, N.; Ben Ayed, M.; Masmoudi, A.; Dhouib, M.; Abdelmoula, M.; Mahfoudh, N.; Makni, H.; Turki, H.; Masmoudi, H.
• Other Names: Cervellati Carlo Academic Editor.
• Is Part Of: Mediators of inflammation. Volume 2018(2018)
• Publication Date: 2018-07-12
• Subjects: Inflammation -- Mediators -- Periodicals; Biological response modifiers -- Periodicals; Inflammation (Pathologie) -- Médiateurs; Immunomodulateurs; Biological response modifiers; Inflammation -- Mediators; Immunology; Autacoids; Immunologic Factors; Cell Adhesion Molecules; Cell Communication; Cytokines; Inflammation; Periodicals; Electronic journals; 616.0473
• DOI: 10.1155/2018/8206983
• Languages: English
• ISSNs: 0962-9351

Abstract

Abstract : Pemphigus foliaceus (PF) is a rare autoimmune skin disease caused by anti-Dsg1 pathogenic autoantibodies. It is considered as a Th2-mediated disease. Likewise, Th17 cells were recently described in the pathogenesis of the disease but their role is still unclear. We aimed to unravel the eventual implication of the IL23/Th17 pathway in the development of PF. A case-control study was conducted on 115 PF patients and 201 healthy controls using PCR-RFLP and AS-PCR methods. SNPs in IL23R, RORγt, IL17A, IL17F, IL17AR, TNFa, and STAT3 genes were genotyped. mRNA expression of IL23R and RORγt was evaluated using Q-PCR. The frequency of circulating Th17 cells was analyzed by flow cytometry. Genetic associations between IL23R >rs11209026, IL17A >rs3748067, IL17F >rs763780, and TNFa >rs1800629 and the susceptibility to PF were reported. Moreover, we revealed a significant increased frequency of circulating CD4 + IL17 + cells as well as higher mRNA levels of ROR γ t and IL23R in PBMCs of patients. However, no significant increase of ROR γ t and IL23R mRNA expression was observed in lesional skin biopsies. In spite of the little size of specimens, our results provide converging arguments for the contribution of the IL23/Th17 pathway in the pathogenesis of PF.