FPR1是宿主免疫细胞上的瘟疫受体
Patrick Osei-Owusu1,2, Thomas M Charlton1,2, Hwan Keun Kim1,2
1Howard Taylor Ricketts Laboratory, Argonne National Laboratory, Lemont, IL, USA.
Nature
|September 20, 2019
概括
瘟疫细菌 (Yersinia pestis) 使用一种特定的蛋白质 (LcrV) 通过N-甲基受体 (FPR1) 向免疫细胞. 阻断或突变FPR1可以防止瘟疫,这表明它在宿主防御中的作用.
科学领域:
- 免疫学
- 微生物学
- 遗传学
背景情况:
- 瘟疫通过使用III型分泌系统破坏免疫细胞引起瘟疫.
- 这种免疫细胞破坏的特定宿主因素以前是未知的.
研究的目的:
- 在感染期间识别Y. pestis的宿主受体.
- 研究这种受体在瘟疫发病和宿主生存中的作用.
主要方法:
- 研究了Y. pestis LcrV蛋白与人类免疫细胞之间的相互作用.
- 用Fpr1缺乏的小鼠来评估对瘟疫的生存和免疫反应.
- 对人类群体进行了FPR1遗传变异的查.
主要成果:
- 在人体免疫细胞上,LcrV与N-甲基受体 (FPR1) 结合,促进细菌效应物的传递.
- 缺乏Fpr1的小鼠表现出更高的生存率和对瘟疫的保护性抗体反应.
- 鉴定了一种人类FPR1变种 (FPR1R190W),该变种对Y. pestis介导的免疫细胞破坏具有抗性.
结论:
- 在小鼠和人类中,FPR1充当Y. pestis的关键受体.
- 缺乏FPR1或特定突变可对瘟疫提供显著的保护.
- 瘟疫可能影响了FPR1基因的演变,影响了人类对其他疾病的免疫力.
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