Herpes simplex virus type 1 activates murine natural interferon-producing cells through toll-like receptor 9
Herpes simplex virus type 1 activates murine natural interferon-producing cells through toll-like receptor 9
复制标题
DOI：
10.1182/blood-2003-08-2674
复制
发表时间：
2004-02-15
期刊：
影响因子：
20.3
通讯作者：
Colonna, M
中科院分区：
文献类型：
--
作者：
Krug, A;Luker, GD;Colonna, M
天然干扰素产生细胞（IPC）专门生产高水平的1型干扰素（IFN），以响应封装的DNA和RNA病毒。在这里，我们证明，1型干扰素的分泌，在响应单纯疱疹病毒1型（HSV-1）在体外介导的Toll样受体9（TLR 9）/MyD 88途径。此外，IPC在体外响应HSV-1产生白细胞介素-12（IL-12），这也依赖于TLR 9/MyD 88信号传导。值得注意的是，尽管TLR 9/MyD 88缺陷在体外消除了对HSV-1的IPC应答，但缺乏MyD 88或TLR 9的小鼠能够在局部感染后控制HSV-1的体内复制，这表明除了IPC之外的细胞中的TLR 9和MyD 88非依赖性途径可以有效地补偿对HSV-1的IPC应答缺陷。
Natural interferon-producing cells (IPCs) specialize in the production of high levels of type 1 interferons (IFNs) in response to encapsulated DNA and RNA viruses. Here we demonstrate that the secretion of type 1 IFN in response to herpes simplex virus type 1 (HSV-1) in vitro is mediated by the toll-like receptor 9 (TLR9)/MyD88 pathway. Moreover, IPCs produce interleukin-12 (IL-12) in response to HSV-1 in vitro, which is also dependent on TLR9/ MyD88 signaling. Remarkably, though TLR9/MyD88-deficiency abrogates IPC responses to HSV-1 in vitro, mice lacking either MyD88 or TLR9 are capable of controlling HSV-1 replication in vivo after local infection, demonstrating that TLR9 and MyD88-Independent pathways in cells other than IPCs can effectively compensate for defective IPC responses to HSV-1.