Association of Serum IL-17A and IL-23 Levels With Alopecia Areata: A Cross-Sectional Comparative Study

Alopecia areata (AA) is an autoimmune, non-scarring hair loss disorder in which T helper 17 (Th17) cells play a key role. Interleukin-23 (IL-23) promotes the differentiation and expansion of Th17 cells from naïve CD4+ T cells. This study aimed to evaluate the association between serum IL-17A and IL-23 levels and disease severity in patients with AA.

A cross-sectional comparative study was conducted at the Department of Dermatology and Venereology, Bangladesh Medical University, Dhaka, from October 2022 to September 2024. Forty-three AA patients and 43 age- and sex-matched healthy controls were enrolled. Serum IL-17A and IL-23 levels were measured using enzyme-linked immunosorbent assay (ELISA) (Elabscience, USA). Disease severity was assessed using the Severity of Alopecia Tool (SALT) score. Data were analyzed with IBM SPSS Statistics for Windows, Version 26 (released 2018; IBM Corp., Armonk, New York, United States) using chi-square, t-test, Mann-Whitney U, and Spearman's correlation tests, with p<0.05 considered statistically significant.

Serum IL-17A and IL-23 levels were significantly higher in AA patients than controls (IL-17A: 39.4 ± 38.3 vs. 13.7 ± 10.7 pg/mL; IL-23: 48.2 ± 57.0 vs. 15.5 ± 15.5 pg/mL; both p<0.001). IL-17A correlated positively with disease severity (p=0.016), increasing from 21.17 ± 33.26 pg/mL in mild cases (S1, <25% hair loss) to 63.47 ± 50.33 pg/mL in severe cases (S4, 75-99% hair loss). IL-17A levels varied across clinical subtypes (single patch: 20.70 ± 24.46 pg/mL; sisaipho: 53.37 ± 1.33 pg/mL; p=0.044). IL-23 levels remained elevated regardless of disease severity (p=0.118) or clinical subtype (p=0.378). A significant positive correlation existed between IL-17A and IL-23 (p<0.001).

Elevated IL-17A levels are associated with AA severity and differ across clinical subtypes, suggesting a role in disease progression and phenotype variation. IL-23 is consistently elevated in AA, highlighting its potential as a biomarker for disease activity. These findings provide insight into cytokine dysregulation in AA and may inform future therapeutic strategies.