Type I interferon induction pathway, but not released interferon, participates in the maturation of dendritic cells induced by negative-strand RNA viruses
Type I interferon induction pathway, but not released interferon, participates in the maturation of dendritic cells induced by negative-strand RNA viruses
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DOI：
10.1086/368381
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发表时间：
2003-04-01
影响因子：
6.4
通讯作者：
Moran, TM
中科院分区：
文献类型：
--
作者：
López, CB;García-Sastre, A;Moran, TM
Toll样受体是细菌和其他病原体诱导的树突状细胞成熟所必需的信号通路。病毒诱导DC成熟的机制尚不清楚。通过使用不同能力的活病毒对诱导干扰素途径，DC成熟与病毒诱导I型干扰素合成的能力有很强的相关性。分泌的干扰素不是必需的，也不足以诱导完全的DC成熟。在这一过程中，细胞内病毒复制是必需的，而转录因子核因子-kappaB在细胞因子诱导中起着关键作用。双链RNA依赖的蛋白激酶不是DC成熟所必需的。与TLR诱导的DC成熟类似，在病毒感染后，诱导细胞因子分泌和主要组织相容性复合体和共刺激分子上调的单独途径被激活。研究表明，这些通路对病毒刺激的存在具有不同的敏感性。
Signaling through toll-like receptors (TLRs) is essential for dendritic cell ( DC) maturation induced by bacteria and other pathogens. The mechanism for virus-induced DC maturation is not known. By use of pairs of live viruses with different abilities to induce the interferon (IFN) pathway, a strong correlation between DC maturation and the ability of the virus to induce type I IFN synthesis was demonstrated. The secreted IFN was not necessary, nor was it sufficient to induce full DC maturation. Intracellular viral replication is necessary for this process, and the transcription factor nuclear factor-kappaB was crucial for cytokine induction. The double-stranded RNA-dependent protein kinase was not essential for DC maturation. Similar to TLR-induced DC maturation, after virus infection, separate pathways for the induction of cytokine secretion and the upregulation of major histocompatibility complex and costimulatory molecules were activated. It was demonstrated that these pathways have different sensitivities to the presence of viral stimulus.