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埃茨1和IL17RA合作调节自身免疫反应和皮肤免疫力对金黄色葡萄球菌

Michael Battaglia¹, Alex C Sunshine¹, Wei Luo¹

¹Department of Biochemistry, State University of New York at Buffalo, Buffalo, NY, United States.

Frontiers in immunology

|September 11, 2023

概括

缺少Ets1的小鼠会产生自身免疫,而IL-17信号受损会使这种情况恶化. 综合的缺陷还导致免疫缺陷和对葡萄球菌感染的敏感性增加,突出显示了复杂的免疫相互作用.

科学领域:

免疫学免疫学免疫学
这是自身免疫力.
传染性疾病传染性疾病

背景情况:

Ets1是一种转录因子,对淋巴细胞功能至关重要.
缺乏 Ets1 的小鼠会发展出具有自身抗体的自身免疫性疾病.
来自Ets1 KO小鼠的原始CD4+T细胞很容易分化为IL-17分泌的Th17细胞.

研究的目的:

调查增加IL-17的产生是否有助于Ets1 KO小鼠的自身免疫.
评估联合Ets1和IL-17受体A (IL17RA) 缺乏对自身免疫表型和免疫功能的影响.
探索IL-17信号传递和树突性表皮T细胞 (DETCs) 在对抗葡萄球菌感染的宿主防御中的作用.

主要方法:

产生双重淘汰赛 (DKO) 的小鼠缺乏Ets1和IL17RA.
使用ELISA,ELISpot,免疫光和流细胞计的DKO和对照小鼠的综合免疫学评估.
皮肤转录组的RNA测序和实验性金黄色葡萄球菌感染模型.

主要成果:

缺少IL17RA信号,在Ets1 KO小鼠中加剧了自身免疫,增加了激活的B细胞和自身抗体.
DKO小鼠表现出免疫缺陷的迹象,包括对葡萄球菌感染和自发皮肤病变的敏感性.
缺少Ets1导致了DETCs的完全丧失,并将DETC缺陷与IL-17信号受损损害的Staphylococcus清除.

结论:

失去IL-17信号增强了Ets1缺乏小鼠的自身免疫力.
伤口愈合的缺陷,如DETC损失,可以与受损的IL-17反应合作,增加对葡萄球菌皮肤感染的易感性.
这些发现揭示了Ets1,IL-17信号传递和免疫防御机制之间的复杂相互作用.

关键词:

在 ETS1 系统中,这就是IL17RARA.黄金葡萄球菌黄金葡萄球菌这是自抗体的自抗体.这是自身免疫力.树突性表皮T细胞免疫缺陷是一种免疫缺陷.

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