微生物诱导的I型干扰素指示树突细胞的平衡基底状态
Laura Schaupp1, Sabine Muth2, Leif Rogell3
1Laboratory of Innate Immunity, Department of Microbiology, Infectious Diseases and Immunology, Charité-Universitätsmedizin Berlin, Hindenburgdamm 30, 12203 Berlin, Germany; Berlin Institute of Health (BIH), Anna-Louisa-Karsch Strasse 2, 10178 Berlin, Germany; Mucosal and Developmental Immunology, Deutsches Rheuma-Forschungszentrum, Charitéplatz 1, 10117 Berlin, Germany; Institute for Molecular Biology (IMB), Ackermannweg 4, 55128 Mainz, Germany.
Cell
|May 8, 2020
概括
肠道微生物群对免疫细胞进行防御. 然而,这种免疫训练可能会导致T细胞对身体自身组织的激活,
科学领域:
- 免疫学
- 微生物学
- 主体与微生物的相互作用
背景情况:
- 环境信号,包括来自微生物群的信号,影响宿主生理和免疫准备.
- 传统的树突细胞 (cDC) 需要微生物群的线索来进行适当的编程以启动适应性免疫力.
- 微生物引导免疫细胞编程的分子机制在很大程度上是未知的.
研究的目的:
- 研究本地微生物群如何控制免疫细胞功能,特别是血细胞DC产生的I型干扰素.
- 阐明微生物群诱导的免疫细胞编程的分子基础及其对宿主防御和耐受性的影响.
主要方法:
- 全基因组转录和表观遗传规律分析.
- 从无细菌和干扰素α/β受体 (IFNAR) 缺乏的小鼠的cDCs的比较.
主要成果:
- 本地微生物群通过血细胞DC调节构成性I型干扰素 (IFN- I) 的产生.
- 性IFNAR信号在cDC中建立特定的表观基因和代谢状态,为病原体接触做好准备.
- 这种免疫指令带有权衡:受指导的cDC可以促进T细胞对自身抗原的反应,可能会损害周围耐受性.
结论:
- 宿主微生物群在培养免疫细胞,平衡病原体防御与自我耐受性方面发挥着至关重要的作用.
- 通过IFNAR信号驱动的微生物驱动的免疫编程会产生一种高度免疫准备状态,但会带来自身免疫的风险.
- 这些发现提供了关于脊椎动物适应其微生物共生者的进化妥协的见解.
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