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Expression of the JAK/STAT Signaling Pathway in Bullous Pemphigoid and Dermatitis Herpetiformis

K Juczynska1, A Wozniacka1, E Waszczykowska1

  • 1Department of Dermatology and Venereology, Medical University of Lodz, Lodz, Poland.

Mediators of Inflammation
|December 6, 2017
PubMed

Insights

Janus kinases (JAK) and signal transducers and activators of transcription (STAT) pathways are upregulated in skin lesions of dermatitis herpetiformis (DH) and bullous pemphigoid (BP) patients, indicating their role in autoimmune bullous diseases.

Area of Science:

  • Immunology
  • Dermatology
  • Molecular Biology

Background:

  • The Janus kinases (JAK) and signal transducers and activators of transcription (STAT) pathway is crucial for cytokine signaling and gene transcription.
  • Dysregulation of the JAK/STAT pathway is implicated in various autoimmune diseases.
  • The role of JAK/STAT signaling in autoimmune bullous diseases, such as dermatitis herpetiformis (DH) and bullous pemphigoid (BP), remains largely unexplored.

Purpose of the Study:

  • To investigate the expression and localization of JAK and STAT proteins in skin lesions of DH and BP patients.
  • To compare protein expression in lesional skin, perilesional skin, and healthy control skin.
  • To elucidate the potential involvement of the JAK/STAT pathway in the pathogenesis of DH and BP.

Main Methods:

  • Immunohistochemistry and immunoblotting were employed to examine JAK and STAT protein expression.
  • Skin biopsies were obtained from 21 DH patients, 20 BP patients, and 10 healthy volunteers.
  • Analysis focused on the differential expression in lesional versus perilesional skin and controls.

Main Results:

  • Significantly elevated expression of JAK/STAT proteins was observed in the skin lesions of both BP and DH patients compared to perilesional skin and healthy controls.
  • These findings suggest a correlation between JAK/STAT pathway activation and the inflammatory processes in autoimmune bullous diseases.
  • Differential expression patterns may relate to specific cytokine activation and the type of inflammatory infiltrate (neutrophilic/eosinophilic).

Conclusions:

  • The JAK/STAT signaling pathway is actively involved in the pathogenesis of dermatitis herpetiformis and bullous pemphigoid.
  • Upregulation of JAK/STAT proteins in lesional skin highlights their contribution to the inflammatory milieu.
  • Further research into JAK/STAT modulation could offer novel therapeutic strategies for autoimmune bullous diseases.

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