IFN受体2 调节TNF-α介导的有害炎症在阿斯伯吉勒斯肺部感染期间
Agnieszka Rynda-Apple1, Jazmin Reyes Servin2, Julianna Lenz2
1Department of Microbiology and Cell Biology, Montana State University, Bozeman, MT.
缺少I型干扰素受体2 (IFNAR2) 在Aspergillus fumigatus感染期间加剧肺损伤和炎症,增加易感性. 中和TNF-α在Ifnar2-/-小鼠中部分恢复了正常反应.
科学领域:
- 免疫学 免疫学 免疫学
- 菌类学 菌类学是指菌类学.
- 肺部病理学 肺部病理学
背景情况:
- 在患有严重流感或SARS-CoV-2的患者中,侵入性肺阿斯伯吉洛症 (IPA) 发生率上升.
- 抗病毒免疫反应可能会创造一个允许真菌感染的肺部环境.
- 缺少I型干扰素受体2亚单元 (IFNAR2) 在允许免疫环境中通过损伤反应调节.
研究的目的:
- 为了研究IFNAR2在宿主易受Aspergillus fumigatus的作用.
- 为了确定IFNAR2缺失是否有助于阿斯伯吉路斯烟草-宽容的肺环境.
主要方法:
- 在没有IFNAR2和IFNAR1.1的情况下,利用小鼠模型研究Aspergillus fumigatus挑战的影响.
- 评估了炎症,发病率,肺损伤和真菌清除.
- 研究了中和TNF-α对Ifnar2-/-小鼠宿主反应的影响.
主要成果:
- 缺少IFNAR2,但没有IFNAR1,导致A. fumigatus挑战后肺炎,发病率和损伤增加.
- 如果nar2-/-小鼠表现出增强的早期状体清除,但仍然发展出侵袭性疾病.
- 在Ifnar2-/-小鼠中中和TNF-α降低了发病率,并将真菌清除正常化到野生类型水平.
结论:
- IFNAR2在调节宿主对A. fumigatus.损害反应方面发挥着至关重要的作用.
- IFNAR2通过调节炎症,特别是TNF-α介导反应,为A. fumigatus允许的环境做出贡献.
- 针对TNF-α可能是一个治疗策略,用于管理特定情况下的IPA.
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