AUTHOR=Chieosilapatham Panjit , Daroontum Teerada , Suwansirikul Songkiet , Chaiwarith Romanee , Phinyo Phichayut , Chaowattanapanit Suteeraporn , Choonhakarn Charoen , Kiratikanon Salin , Rujiwetpongstorn Rujira , Tovanabutra Napatra , Chiewchanvit Siri , Chuamanochan Mati TITLE=Comparative immunohistochemical analysis of inflammatory cytokines in distinct subtypes of Sweet syndrome JOURNAL=Frontiers in Immunology VOLUME=Volume 15 - 2024 YEAR=2024 URL=https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2024.1355681 DOI=10.3389/fimmu.2024.1355681 ISSN=1664-3224 ABSTRACT=Background

A 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.

Objective

To investigate alterations in inflammatory cytokines in skin lesions of distinct subtypes of SS.

Methods

Skin 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.

Results

The 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.

Conclusions

These 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.