RNA modification in immune evasion and immune recognition

RNA修饰在免疫逃避和免疫识别中的作用

• 批准号: 115690894
• 负责人: Professor Dr. Stefan Bauer
• 金额: --
• 依托单位: Institut für Immunologie
• 依托单位国家: 德国
• 项目类别: Research Grants
• 财政年份: 2009
• 资助国家: 德国
• 起止时间: 2008-12-31 至 2011-12-31
• 项目状态: 已结题
• 来源: https://gepris.dfg.de/gepris/projekt/115690894?language=en
• 关键词: RNA; modification; immune; evasion; recognition

The innate immune system senses viral RNA via Toll-like receptors (TLR) and RNA helicases. RNA modifications such as 2’O-ribosemethylation or base methylation (5-methyl-cytidine) render self RNA non-immunostimulatory and are the basis of selfversus viral RNA discrimination. However, the role of self or viral RNA in immunoregulation and immune evasion are not well understood. We have demonstrated that non-modified RNA triggers TLR7, whereas 2’O-ribose methylated RNA blocks immune activation. It is hypothesized that certain RNA viruses methylate their genome by virally encoded 2’O-ribose-methyltransferase (2’O-MTase) to evade immune recognition. Furthermore, our data suggest that viral infection or in vitro digestion with single-strand-specific RNase A renders self RNA immunostimulatory. The goal of the project is to discover and define novel basic viral and host immune mechanisms. They will provide a more sophisticated understanding of the immune response to virus infection and may lead to new adjuvant for future vaccine and therapeutic antiviral drug development.

先天免疫系统通过Toll样受体(TLR)和RNA解旋酶感知病毒RNA。RNA修饰，如2‘O-核糖甲基化或碱基甲基化(5-甲基胞苷)使自身RNA无免疫刺激作用，是区分自身和病毒RNA的基础。然而，自身或病毒RNA在免疫调节和免疫逃避中的作用还不是很清楚。我们已经证明，未修饰的RNA触发TLR7，而2‘O-核糖甲基化的RNA阻止免疫激活。假设某些RNA病毒通过病毒编码的2‘O-核糖甲基转移酶(2’O-MTase)甲基化其基因组以逃避免疫识别。此外，我们的数据表明，病毒感染或单链特异性RNase A的体外消化使自身RNA具有免疫刺激作用。该项目的目标是发现和定义新的基本病毒和宿主免疫机制。它们将对病毒感染的免疫反应提供更复杂的理解，并可能为未来的疫苗和治疗性抗病毒药物开发提供新的佐剂。

项目成果

Detection of RNA Modifications by HPLC Analysis and Competitive ELISA

通过 HPLC 分析和竞争性 ELISA 检测 RNA 修饰

• DOI: 10.1007/978-1-4939-0882-0_1
• 发表时间: 2014
• 期刊: Innate DNA and RNA Recognition
• 作者: A. Kaufmann;S. Bauer
• 通讯作者: S. Bauer