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

Hilal Ayvaz Celik1, Nilgun Gurbuz2, Ergin Turantepe2

  • 1Department of Dermatology, Faculty of Medicine, Suleyman Demirel University, Isparta, Türkiye.

Dermatology Practical & Conceptual
|December 9, 2024
PubMed
Abstract

Insights

Toll-like receptors (TLR) and specific cytokines are elevated in morphea patients, suggesting their role in localized scleroderma pathogenesis. This finding may guide future TLR-targeted therapies for morphea.

Area of Science:

  • Dermatology
  • Immunology
  • Pathogenesis of Fibrotic Diseases

Background:

  • Morphea, or localized scleroderma, is a rare inflammatory fibrotic skin condition with an unclear cause.
  • Research on the role of Toll-like receptors (TLR) in morphea pathogenesis is limited.

Purpose of the Study:

  • To investigate Toll-like receptor (TLR) expression in morphea lesions.
  • To quantify serum levels of IL-6, IL-17A, TGF-β1, FGF, and VEGF in morphea patients.
  • To compare these levels with those in healthy individuals.

Main Methods:

  • Gene expression analysis using RT-PCR for TLRs in lesional and non-lesional skin.
  • Enzyme-linked immunosorbent assay (ELISA) for serum cytokine and growth factor quantification.
  • Comparative analysis between morphea patients and healthy controls.

Main Results:

  • Significantly increased TLR1 gene expression (34.3-fold) was observed in lesional skin of morphea patients.
  • Elevated serum levels of IL-6, IL-17A, TGF-β1, FGF, and VEGF were detected in patients compared to controls.
  • These findings indicate a potential inflammatory and fibrotic pathway involvement.

Conclusions:

  • Toll-like receptors (TLR) play a crucial role in the pathogenesis of morphea.
  • Understanding TLR involvement can lead to more targeted and effective morphea treatments.
  • This study supports the development of novel TLR-targeted therapeutic strategies for localized scleroderma.

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