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Background <p>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.</p> Methods <p>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.</p> Results <p>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, <i>p</i> = 0.002). Conversely, rs2201841 increased psoriasis risk (OR = 1.39, <i>p</i> = 0.001), as did rs7530511 under the recessive model (OR = 1.29, <i>p</i> = 0.014). Significant associations were found between polymorphisms and both psoriasis severity (<i>p</i> &lt; 0.001) and clinical type (<i>p</i> &lt; 0.001).</p> Conclusion <p>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.</p>

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

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月18日

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  • Saboor Ahmadipanah,
  • Parand Shariat Rad,
  • Maryam Montaseri,
  • Houshang Nemati,
  • Masoud Sadeghi,
  • Mazaher Ramezani

摘要

Background

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.

Methods

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.

Results

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).

Conclusion

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.