已发表论文

基于组蛋白修饰确定治疗过敏性鼻炎的新靶点

 

Authors Li H , Wang R, Yu B, Zeng J, Xiao Z

Received 6 June 2025

Accepted for publication 10 October 2025

Published 27 October 2025 Volume 2025:18 Pages 14971—14987

DOI https://doi.org/10.2147/JIR.S535690

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Prof. Dr. Yuhan Xing

Hanqiao Li,1– 3 Renkang Wang,1– 3 Benquan Yu,1– 3 Junjie Zeng,1– 3 Zian Xiao1– 3 

1Department of Otorhinolaryngology Head and Neck Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan Province, People’s Republic of China; 2Institute of Otology, Central South University, Changsha, Hunan Province, People’s Republic of China; 3Laboratory of Otorhinolaryngology Head and Neck Cancer, The Second Xiangya Hospital, Central South University, Changsha, Hunan Province, People’s Republic of China

Correspondence: Zian Xiao, Department of Otorhinolaryngology Head and Neck Surgery, The Second Xiangya Hospital, Central South University, Changsha, 410011, Hunan Province, People’s Republic of China, Email xiaozian@csu.edu.cn
摘要

目的:

组蛋白修饰在其他气道过敏性疾病发生发展中的作用已被广泛研究,但在变应性鼻炎(AR)中的作用尚未被深入探讨。

方法:

从基因表达综合数据库下载GSE50223数据集,通过FACER数据库获取组蛋白修饰相关基因,并利用加权基因共表达网络分析和单细胞测序分析筛选AR中与组蛋白修饰相关的关键功能基因。最后收集AR患者及健康人群的鼻黏膜组织进行目标基因表达验证。在功能层面,建立屋尘螨致敏的人鼻上皮细胞与初始CD4 T细胞的共培养体系,通过基因敲低和过表达技术分析SIN3ATh17Treg细胞分化中的作用。

结果:

SIN3A被鉴定为AR中差异表达的组蛋白修饰关键功能基因,单细胞数据分析显示SIN3A可能通过调节Treg细胞参与免疫浸润差异。在AR患者鼻黏膜组织中证实SIN3A表达上调。功能实验表明SIN3A促进初始T细胞向Th17分化并抑制其向Treg细胞分化,从而破坏Th17/Treg平衡。

结论:

组蛋白修饰相关基因SIN3AAR与健康人群中存在差异表达。SIN3A可能通过调控Th17/Treg免疫平衡在AR发病机制中发挥重要作用。本研究首次揭示SIN3A介导变应性鼻炎免疫失衡的新型表观遗传机制,为开发靶向SIN3A的干预策略提供理论依据。