Serum IL-36 Cytokine Profile in Adult Patients With Acne Vulgaris: A Case–Control Study
Dermatologic Therapy, cilt.2026, sa.1, 2026 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 2026 Sayı: 1
- Basım Tarihi: 2026
- Doi Numarası: 10.1155/dth/9892983
- Dergi Adı: Dermatologic Therapy
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, EMBASE, Academic Search Ultimate (EBSCO), Biomedical Reference Collection: Corporate Edition (EBSCO), Health Research Premium Collection (ProQuest)
- Anahtar Kelimeler: acne vulgaris, cytokines, inflammation, interleukin-36 alpha, interleukin-36 receptor antagonist
- Ankara Yıldırım Beyazıt Üniversitesi Adresli: Evet
Özet
Introduction and Objective: Acne vulgaris (AV) is a chronic inflammatory disease of the pilosebaceous unit characterized by complex immunological mechanisms. The interleukin-36 (IL-36) cytokine family has been implicated in various inflammatory skin disorders; however, its role in adult AV remains insufficiently defined. This study aimed to evaluate serum IL-36 cytokine profiles in adult AV patients and to investigate their associations with demographic and clinical characteristics. Materials and Methods: This cross-sectional case–control study included 70 adult AV patients and 70 healthy controls. Serum levels of IL-36α, IL-36β, IL-36γ, and the IL-36 receptor antagonist (IL-36Ra) were measured using ELISA. Demographic data (including BMI, smoking, and alcohol status), disease severity, duration, and treatment history were recorded. Group differences were evaluated using adjusted and unadjusted analyses. Results: Serum IL-36α levels were significantly higher, whereas IL-36Ra levels were significantly lower in AV patients compared to controls (adjusted p = 0.011 and p < 0.001, respectively). Although IL-36β levels were lower in unadjusted analyses, this difference was not significant after covariate adjustment. No significant difference was observed for IL-36γ. IL-36Ra demonstrated the highest discriminative ability (AUC = 0.717), followed by IL-36α (AUC = 0.642). No consistent associations were identified between IL-36 cytokines and disease severity or clinical parameters after correction for multiple testing. The differences in IL-36α and IL-36Ra remained significant after adjustment for confounders. Conclusion: This study demonstrates an imbalance in IL-36 cytokine profiles in adult AV patients, characterized by elevated IL-36α and reduced IL-36Ra levels. These findings suggest a potential role for IL-36-mediated pathways in the inflammatory milieu of AV, although further prospective studies with tissue-level analyses are needed to clarify their pathophysiological relevance.