IL-23 serum levels and IL23R polymorphisms in psoriasis: a meta-analysis of susceptibility and severity

Psoriasis is an immune-mediated inflammatory disease with a strong genetic basis. The Interleukin-23 (IL-23)/Th17 axis is central to its pathogenesis. While IL-23 is established, studies on systemic serum levels and IL23R gene polymorphisms yielded varied results. Our study clarified these associations through a systematic review and meta-analysis. A systematic search was performed to find relevant studies. For serum IL-23, a random-effects model calculated overall Hedges’s g. For polymorphisms, pooled odds ratios (ORs) with 95% confidence intervals (CIs) were calculated for allelic, dominant, and recessive models. Heterogeneity (I² statistic) and sensitivity analyses were performed. Meta-analysis of serum IL-23 levels (six studies) showed no significant difference between patients and controls (Hedges’s g = -0.48, 95% CI: -1.58 to 0.62) with high heterogeneity (I² = 96.34%). For polymorphisms, the rs11209026 A allele showed a significant protective effect (OR = 0.52, p = 0.002). Conversely, rs2201841 increased psoriasis risk (OR = 1.39, p = 0.001), as did rs7530511 under the recessive model (OR = 1.29, p = 0.014). Significant associations were found between polymorphisms and both psoriasis severity (p < 0.001) and clinical type (p < 0.001). Our meta-analysis confirms a significant association between IL23R polymorphisms and susceptibility to psoriasis, with rs11209026 being protective and rs2201841 conferring risk. However, data does not support serum IL-23 as a reliable biomarker. This study widens the view toward personalized medicine and using polymorphisms as prognostic models.