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Purpose <p>To investigate the role of the interleukin-23 (IL-23)/T helper type 17 (Th17) immune axis in conjunctival allergic inflammation using a murine model of experimental allergic conjunctivitis (EAC).</p> Study design <p>Experimental study.</p> Methods <p>BALB/c mice were assigned to four groups: control (untreated), allergy (EAC), IL-23 (EAC with IL-23 eyelid injection), and non-sensitized IL-23 (non-sensitized with IL-23 eyelid injection). Conjunctival tissue was analyzed histologically to quantify eosinophil and neutrophil infiltration. Gene expression of mRNA in conjunctival tissue was assessed using a PCR array and quantitative RT-PCR.</p> Results <p>Eosinophilic and neutrophilic infiltration in the subconjunctival tissue was more pronounced in the IL-23 group than in the allergy and control groups. PCR array and quantitative RT-PCR analyses revealed significantly elevated <i>Ccl17/Tarc</i> mRNA expression in the IL-23 group compared to the allergy group. <i>IL-17A</i> mRNA, undetectable in the allergy group, was expressed in the IL-23 group. Additionally, PCR array comparisons between the IL-23 and non-sensitized IL-23 groups showed a significant increase in <i>Rorc</i> and <i>Il1r1</i> expression in the IL-23 group. At the same time, <i>Mmp3</i>, <i>Ccl7</i>, and <i>Ccr2</i> were significantly upregulated in the non-sensitized IL-23 group. RT-PCR analysis also demonstrated higher <i>IL-17A</i> mRNA levels in the non-sensitized IL-23 group than in the IL-23 group.</p> Conclusion <p>IL-23 induces mixed eosinophilic–neutrophilic inflammation in conjunctival tissue, characterized by enhanced Th2 and weak Th17 responses in a murine model of EAC. These findings suggest a modulatory role of the IL-23/Th17 axis in influencing the severity and phenotype of allergic conjunctival inflammation.</p>

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Conjunctival allergic inflammation involving the interleukin-23/T helper type 17 immune axis in an experimental allergic conjunctivitis mouse model

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月13日

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  • Rumi Adachi,
  • Jun Shoji,
  • Noriko Inada,
  • Akiko Tomioka,
  • Satoru Yamagami

摘要

Purpose

To investigate the role of the interleukin-23 (IL-23)/T helper type 17 (Th17) immune axis in conjunctival allergic inflammation using a murine model of experimental allergic conjunctivitis (EAC).

Study design

Experimental study.

Methods

BALB/c mice were assigned to four groups: control (untreated), allergy (EAC), IL-23 (EAC with IL-23 eyelid injection), and non-sensitized IL-23 (non-sensitized with IL-23 eyelid injection). Conjunctival tissue was analyzed histologically to quantify eosinophil and neutrophil infiltration. Gene expression of mRNA in conjunctival tissue was assessed using a PCR array and quantitative RT-PCR.

Results

Eosinophilic and neutrophilic infiltration in the subconjunctival tissue was more pronounced in the IL-23 group than in the allergy and control groups. PCR array and quantitative RT-PCR analyses revealed significantly elevated Ccl17/Tarc mRNA expression in the IL-23 group compared to the allergy group. IL-17A mRNA, undetectable in the allergy group, was expressed in the IL-23 group. Additionally, PCR array comparisons between the IL-23 and non-sensitized IL-23 groups showed a significant increase in Rorc and Il1r1 expression in the IL-23 group. At the same time, Mmp3, Ccl7, and Ccr2 were significantly upregulated in the non-sensitized IL-23 group. RT-PCR analysis also demonstrated higher IL-17A mRNA levels in the non-sensitized IL-23 group than in the IL-23 group.

Conclusion

IL-23 induces mixed eosinophilic–neutrophilic inflammation in conjunctival tissue, characterized by enhanced Th2 and weak Th17 responses in a murine model of EAC. These findings suggest a modulatory role of the IL-23/Th17 axis in influencing the severity and phenotype of allergic conjunctival inflammation.