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在牙周炎期间的Th17-to-Tfh可塑性限制了疾病病理学

Flora A McClure¹, Kelly Wemyss¹, Joshua R Cox¹

¹Lydia Becker Institute of Immunology and Inflammation, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, The University of Manchester , Manchester, UK.

The Journal of experimental medicine

|May 31, 2024

概括

在牙周炎中探索了Th17细胞可塑性,在炎症中至关重要. 一些Th17细胞转移到淋巴结中的Tfh细胞,这一过程通过增强口腔免疫力来限制疾病的严重程度.

科学领域:

免疫学免疫学免疫学
微生物学微生物学
牙周病研究牙周病研究

背景情况:

Th17细胞的可塑性与自身炎症性疾病有关.
牙周炎涉及Th17细胞,但它们在这种情况下的可塑性是未知的.

研究的目的:

在牙周炎期间调查Th17细胞的功能可塑性.
确定Th17细胞可塑性在牙周炎病理学中的作用.

主要方法:

在牙周炎模型中利用IL-17命运映射.
分析了T细胞细胞因子的产生和表型在牙和排水淋巴结.
评估了Th17-to-Tfh可塑性对牙周骨损失,IgG水平和口腔微生物群的影响.

主要成果:

在牙周炎期间,牙周Th17细胞在很大程度上保留了IL-17A的产生.
在排水淋巴结中的IL-17表达T细胞表现出可塑性,分化为Tfh类细胞.
这种依赖IL-6的Th17-to-Tfh可塑性具有保护性,限制骨损失和控制口腔开始性细菌.

结论:

Th17细胞可塑性发生在牙周炎中,特别是淋巴结中的Th17-to-Tfh细胞切换.
这种可塑性通过增强口腔免疫力和限制牙周病而起保护作用.
致病的Th17细胞的一个子集可以通过可塑性获得保护功能.

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