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Profiling of Toll-like Receptors and Related Signaling Mediators in the Pathogenesis of Morphea

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dc.creator Celik, Hilal Ayvaz
dc.creator Secme, Mücahit
dc.creator Dodurga, Yavuz
dc.creator Turantepe, Ergin
dc.creator GÜRBÜZ, Nilgün
dc.date 2024-10-01T00:00:00Z
dc.date.accessioned 2025-02-25T10:16:31Z
dc.date.available 2025-02-25T10:16:31Z
dc.identifier 057985a8-b49d-4f4e-ab2a-7ed2580fc56f
dc.identifier 10.5826/dpc.1404a219
dc.identifier https://avesis.sdu.edu.tr/publication/details/057985a8-b49d-4f4e-ab2a-7ed2580fc56f/oai
dc.identifier.uri http://acikerisim.sdu.edu.tr/xmlui/handle/123456789/98826
dc.description 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-β1, 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-β1, 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-β, 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.
dc.language eng
dc.rights info:eu-repo/semantics/closedAccess
dc.title Profiling of Toll-like Receptors and Related Signaling Mediators in the Pathogenesis of Morphea
dc.type info:eu-repo/semantics/article


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