Contribution of interferon-β to the immune activation induced by double-stranded DNA

被引:24
作者
Shirota, Hidekazu
Ishii, Ken J.
Takakuwa, Hiroki
Klinman, Dennis M.
机构
[1] US FDA, Ctr Biol Evaluat & Res, Sect Retroviral Immunol, Bethesda, MD 20892 USA
[2] US FDA, Ctr Biol Evaluat & Res, Lab DNA Viruses, Bethesda, MD 20892 USA
[3] Osaka Univ, Japan Sci & Technol Agcy, ERATO, Res Inst Microbial Dis,Dept Host Def, Osaka, Japan
关键词
type; 1; IFNs; Toll-like receptor; DNA; host protection;
D O I
10.1111/j.1365-2567.2006.02367.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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.
引用
收藏
页码:302 / 310
页数:9
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