Please use this identifier to cite or link to this item: https://hdl.handle.net/11499/58368
Title: Profiling of Toll-like Receptors and Related Signaling Mediators in the Pathogenesis of Morphea
Authors: Celik, Hilal Ayvaz
Gurbuz, Nilgun
Turantepe, Ergin
Secme, Muecahit
Dodurga, Yavuz
Keywords: morphea
localized scleroderma
toll-like receptors
TLR
growth factors
Systemic-Sclerosis
Localized Scleroderma
Innate
Gene
Expression
Responses
Update
Cells
Tlr9
Ifn
Publisher: Mattioli 1885
Abstract: Introduction: Morphea, also known as localized scleroderma, is a rare fibrosing inflammatory disease of unknown pathogenesis. Objectives: Although the genetic basis for morphea is important, reports on the evaluation of Toll-like receptors (TLR) in this disease is quite limited. We aimed to evaluate TLR expression levels and serum IL-6, IL-17A, TGF-(31, FGF, and VEGF levels in patients with morphea and compare these results with healthy controls. Methods: The expression levels of TLRs in the lesional and non-lesional adjacent skin of patients with morphea and in normal skin of healthy controls were evaluated by RT-PCR, whereas serum levels of IL-6, IL-17A, TGF-(31, FGF, and VEGF were evaluated by ELISA. Results: Based on our findings, TLR1 gene expression increased 34.3-fold in the lesional skin of patients with morphea. In addition, IL-6, IL-17A, TGF-(3, FGF, and VEGF were found to be higher in the blood samples of the patient group than in the healthy group. Conclusion: TLRs are important parts of the pathogenesis of morphea, and a better understanding of them will lead to more directed, effective treatments. We believe that this study will be important for pioneering TLR-targeted therapeutic approaches in the treatment of morphea in the future.
URI: https://doi.org/10.5826/dpc.1404a219
https://hdl.handle.net/11499/58368
ISSN: 2160-9381
Appears in Collections:Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection
Tıp Fakültesi Koleksiyonu
WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection

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