Non-canonical IL-22 receptor signaling remodels the mucosal barrier during fungal immunosurveillance

bioRxiv - Immunology Pub Date : 2024-09-13 DOI:10.1101/2024.09.08.611873

Nicolas Millet, Jinendiran Sekar, Norma V. Solis, Antoine Millet, Felix E.Y. Aggor, Asia Wildeman, Michail S. Lionakis, Sarah L. Gaffen, Nicholas Jendzjowsky, Scott G. Filler, Marc Swidergall

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Abstract

Mucosal barrier integrity is vital for homeostasis with commensal organisms while preventing pathogen invasion. We unexpectedly found that fungal-induced immunosurveillance enhances resistance to fungal outgrowth and tissue invasion by remodeling the oral mucosal epithelial barrier in mouse models of adult and neonatal Candida albicans colonization. Epithelial subset expansion and tissue remodeling were dependent on interleukin-22 (IL-22) and signal transducer and activator of transcription 3 (STAT3) signaling, through a non-canonical receptor complex composed of glycoprotein 130 (gp130) coupled with IL-22RA1 and IL-10RB. Immunosurveillance-induced epithelial remodeling was restricted to the oral mucosa, whereas barrier architecture was reset once fungal-specific immunity developed. Collectively, these findings identify fungal-induced transient mucosal remodeling as a critical determinant of resistance to mucosal fungal infection during early stages of microbial colonization.

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非典型 IL-22 受体信号在真菌免疫监视过程中重塑粘膜屏障

粘膜屏障的完整性对于维持共生生物的平衡和防止病原体入侵至关重要。我们意外地发现，在成年和新生儿白色念珠菌定植小鼠模型中，真菌诱导的免疫监视可通过重塑口腔黏膜上皮屏障来增强对真菌生长和组织入侵的抵抗力。上皮细胞亚群的扩大和组织重塑依赖于白细胞介素-22（IL-22）和信号转导及转录激活因子 3（STAT3）信号，通过糖蛋白 130（gp130）与 IL-22RA1 和 IL-10RB 组成的非经典受体复合物进行。免疫监视诱导的上皮重塑仅限于口腔粘膜，而一旦真菌特异性免疫形成，屏障结构就会重置。总之，这些研究结果表明，真菌诱导的瞬时粘膜重塑是微生物定植早期阶段抵抗粘膜真菌感染的关键决定因素。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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bioRxiv - Immunology

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