Recognition mechanism of DNA by innate immunity

先天免疫对DNA的识别机制

• 批准号: 23689030
• 负责人: KAWAI Taro
• 金额: $ 17.56万
• 依托单位: Nara Institute of Science and Technology (2013)Osaka University (2011-2012)
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Young Scientists (A)
• 财政年份: 2011
• 资助国家: 日本
• 起止时间: 2011-04-01 至 2014-03-31
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-23689030/
• 关键词: 自然免疫; DNAセンサー; シグナル伝達; インターフェロン; ウイルス; 自己免疫疾患; ウイルス感染

Upon recognition of double-stranded DNA derived from virus or bacteria by innate immunity, host cells produce type I interferon or other inflammatory mediators essential for host defense. However, mechanisms involved in DNA recognition are unclear. In addition, it is suggested that self-DNA derived from damaged cells are recognized by innate immunity and this is considered to be responsible for development of inflammatory and autoimmune diseases. In this research, we identified MRE11, a protein involved in repair responses, as a candidate protein involved in self-DNA recognition and induction of type I interferon and inflammatory cytokines. MRE11 binds to and colocalizes with immunostimulatory DNA, and cells that do not express MRE11 have defects in induction of these cytokines by immunostimulatory DNA. These findings may shed light on our understanding of pathogenesis of autoimmunity in which aberrant DNA recognition is involved.

当先天免疫识别来自病毒或细菌的双链DNA时，宿主细胞产生I型干扰素或宿主防御所必需的其他炎症介质。然而，涉及DNA识别的机制尚不清楚。此外，有人认为，来自受损细胞的自身DNA被先天免疫识别，这被认为是导致炎症和自身免疫性疾病发展的原因。在这项研究中，我们确定了MRE 11，一种参与修复反应的蛋白质，作为参与自我DNA识别和诱导I型干扰素和炎性细胞因子的候选蛋白质。MRE 11与免疫刺激性DNA结合并共定位，不表达MRE 11的细胞在通过免疫刺激性DNA诱导这些细胞因子方面存在缺陷。这些发现可能有助于我们理解异常DNA识别参与的自身免疫发病机制。

项目成果

Dissection of signaling pathways through innate receptors that sense foreign nucleic acids

通过感知外源核酸的先天受体剖析信号通路

• 发表时间: 2011
• 作者: 近藤科江;他;Taro Kawai
• 通讯作者: Taro Kawai

The Second Messenger Phosphatidylinositol-5-Phosphate Facilitates Antiviral Innate Immune Signaling

• DOI: 10.1016/j.chom.2013.07.011
• 发表时间: 2013-08-14
• 期刊: CELL HOST & MICROBE
• 影响因子: 30.3
• 作者: Kawasaki, Takumi;Takemura, Naoki;Kawai, Taro
• 通讯作者: Kawai, Taro

Viral infection augments Nod1/2 signaling to potentiate lethality associated with secondary bacterial infections.

• DOI: 10.1016/j.chom.2011.05.006
• 发表时间: 2011-06-16
• 期刊: Cell host & microbe
• 影响因子: 30.3
• 作者: Kim YG;Park JH;Reimer T;Baker DP;Kawai T;Kumar H;Akira S;Wobus C;Núñez G
• 通讯作者: Núñez G

Poly ICのアジュバント効果における細胞死の役割

细胞死亡在 Poly IC 佐剂作用中的作用

• 发表时间: 2013
• 作者: 金田典雄;伊東進 編;河合太郎
• 通讯作者: 河合太郎

免疫学Update

免疫学更新

• 发表时间: 2012
• 作者: 香山尚子;竹田潔
• 通讯作者: 竹田潔