Frontiers in Immunology (Mar 2024)

Comparative immunohistochemical analysis of inflammatory cytokines in distinct subtypes of Sweet syndrome

  • Panjit Chieosilapatham,
  • Panjit Chieosilapatham,
  • Teerada Daroontum,
  • Songkiet Suwansirikul,
  • Romanee Chaiwarith,
  • Phichayut Phinyo,
  • Phichayut Phinyo,
  • Suteeraporn Chaowattanapanit,
  • Charoen Choonhakarn,
  • Salin Kiratikanon,
  • Rujira Rujiwetpongstorn,
  • Napatra Tovanabutra,
  • Siri Chiewchanvit,
  • Mati Chuamanochan,
  • Mati Chuamanochan

DOI
https://doi.org/10.3389/fimmu.2024.1355681
Journal volume & issue
Vol. 15

Abstract

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BackgroundA dysregulated immune response has been implicated in Sweet syndrome (SS) pathogenesis; however, cytokine profiles across different conditions associated with SS — including adult-onset immunodeficiency (AOID) due to anti-interferon (IFN)-γ autoantibodies — remain unknown.ObjectiveTo investigate alterations in inflammatory cytokines in skin lesions of distinct subtypes of SS.MethodsSkin biopsies were collected from 42 AOID- and 52 non-AOID-associated SS patients and 18 healthy controls. The comparative immunohistochemical study was conducted using monoclonal antibodies against interleukin (IL)-1β, IL-6, IL-17, IFN-γ, and tumor necrosis factor-α on paraffin-embedded sections. The quantitative percentage positivity and intensity were calculated using computer-based image analysis.ResultsThe results showed stronger and more diffuse dermal immunoreactivity for IFN-γ and IL-17 in the AOID-associated (p < 0.001 and p < 0.001, respectively) and non-AOID-associated SS (p < 0.001 and p < 0.001, respectively) groups. However, no significant differences in the levels of these two cytokines were observed between the AOID- and non-AOID-associated SS groups. Increased expression of IFN-γ together with IL-17 was also noted in almost all subtypes among non-AOID-associated SS.ConclusionsThese results demonstrate that IFN-γ and IL-17 are implicated in immunopathology of all SS subtypes, including AOID-associated SS, despite the presence of anti-IFN-γ autoantibodies.

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