Shirota Hidekazu, Ishii Ken J, Takakuwa Hiroki, Klinman Dennis M
Section of Retroviral Immunology, Center for Biologics Evaluation and Research, US Food and Drug Administration, Bethesda, MD 20892, USA.
Immunology. 2006 Jul;118(3):302-10. doi: 10.1111/j.1365-2567.2006.02367.x.
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.
将双链DNA（dsDNA）引入巨噬细胞和树突状细胞的细胞质会触发这些专职抗原呈递细胞（APC）的激活。这一过程的特征是共刺激分子上调以及产生各种细胞因子、趋化因子和抗菌/抗病毒因子。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关键作用。免疫细胞和非免疫细胞都会通过上调IFN-β的表达来响应细胞质内的dsDNA，这一过程会降低宿主对感染的易感性。dsDNA诱导的免疫激活不依赖于髓样分化因子88（MyD88）、TIR结构域衔接蛋白诱导干扰素-β（TRIF）和DNA依赖性蛋白激酶催化亚基（DNA-PKcs），这表明细胞质内dsDNA介导的细胞激活是由一种不依赖Toll样受体的机制所驱动的。
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