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作 者:刘意 余曼[2] LIU Yi;YU Man(School of Medicine,University of Electronic Science and Technology of China,Chengdu 610054,China;Department of Ophthalmology,Sichuan Provincial People’s Hospital,University of Electronic Science and Technology of China,Chengdu,China,Chinese Academy of Sciences Sichuan Translational Medicine Research Hospital,Chengdu 610072,China)
机构地区:[1]电子科技大学医学院,成都610054 [2]电子科技大学附属医院四川省人民医院眼科,成都610072
出 处:《中国眼耳鼻喉科杂志》2023年第6期502-506,共5页Chinese Journal of Ophthalmology and Otorhinolaryngology
基 金:国家自然科学基金面上项目(82070829);四川省人民医院“浣花英才计划”(SY2022023);成都市科技局科技项目(2022-YF05-01936-SN)。
摘 要:干眼是一种影响眼表的炎症性自身免疫疾病。近年来,致病效应辅助性T细胞17 (Th17)在干眼发病过程中的关键作用备受关注。Th17细胞通过产生IL-17来拮抗调节性T细胞(Treg),导致Th17细胞进一步扩增以及相关炎症因子的过度表达;在体内阻断IL-17可以减少Th17细胞扩增并促进Treg功能恢复,从而显著降低干眼的严重程度。因此,调控Th17细胞向Treg分化的抗炎药物可有效抑制干眼炎症,有望成为治疗干眼的新型抗炎药物。Dry eye disease(DED)is an inflammatory autoimmune disorder affecting the ocular surface.In recent years,the key role of pathogenic T cells,particularly Th17 cells in the immunopathogenesis of DED has received much attention.IL-17-secreting Th17 cells antagonize the regulatory T cell(Treg)function by facilitating further expansion of Th17 cells and Th17-associated inflammatory factors.In vivo blockade of IL-17 significantly reduces the severity and progression of DED,which is paralleled by a reduction in the expansion of Th17 cells and restoration of Treg function.Therefore,anti-inflammatory drugs that regulate the differentiation of Th17 cells into regulatory T cells can effectively inhibit DED inflammation,which is expected to become a new anti-inflammatory drug for DED.
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