Contribution of interferon-β to the immune activation induced by double-stranded DNA
Contribution of interferon-β to the immune activation induced by double-stranded DNA
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DOI：
10.1111/j.1365-2567.2006.02367.x
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发表时间：
2006-07-01
期刊：
影响因子：
6.4
通讯作者：
Klinman, Dennis M.
中科院分区：
文献类型：
--
作者：
Shirota, Hidekazu;Ishii, Ken J.;Klinman, Dennis M.
将双链DNA（dsDNA）引入巨噬细胞和树突状细胞的细胞质中会触发这些专职抗原递呈细胞（APC）的激活。该过程的特征在于共刺激分子的上调和各种细胞因子、趋化因子和抗菌/病毒因子的产生。目前的研究结果表明，干扰素-β（IFN-β）在dsDNA触发的刺激级联反应中起着关键作用。免疫细胞和非免疫细胞都通过上调IFN-β表达来响应胞质内dsDNA，这是一个降低宿主对感染易感性的过程。dsDNA诱导的免疫激活不依赖于MyD 88、TRIF和DNA-PKcs，表明Toll样受体非依赖性机制是胞浆内dsDNA介导的细胞激活的基础。
Introducing double-stranded DNA (dsDNA) into the cytoplasm of macrophages and dendritic cells triggers the activation of these professional antigen-presenting cells (APCs). This process is characterized by the up-regulation of costimulatory molecules and the production of various cytokines, chemokines, and antibacterial/viral factors. Current findings indicate that interferon-beta (IFN-beta) plays a key role in the stimulatory cascade triggered by dsDNA. Both immune and non-immune cells respond to intracytoplasmic dsDNA by up-regulating IFN-beta) expression, a process that reduces host susceptibility to infection. The immune activation induced by dsDNA is independent of MyD88, TRIF and DNA-PKcs, indicating that a Toll-like receptor-independent mechanism underlies the cellular activation mediated by intracytoplasmic dsDNA.