Interaction between conventional dendritic cells and natural killer cells is integral to the activation of effective antiviral immunity
Interaction between conventional dendritic cells and natural killer cells is integral to the activation of effective antiviral immunity
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DOI：
10.1038/ni1244
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发表时间：
2005-10-01
影响因子：
30.5
通讯作者：
Degli-Esposti, MA
中科院分区：
文献类型：
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作者：
Andoniou, CE;van Dommelen, SLH;Degli-Esposti, MA
树突状细胞（dc）调节先天免疫的各个方面，包括自然杀伤细胞（NK）功能。在这里，我们定义了在病毒感染过程中DC - NK细胞相互作用的机制。小鼠巨细胞病毒（MCMV）感染的CD11b(+) dc有效激活NK细胞。NK细胞的细胞毒性需要干扰素- α和NKG2D激活受体与NKG2D配体之间的相互作用，而NK细胞产生干扰素- γ主要依赖dc衍生的白细胞介素18。虽然toll样受体9有助于抗病毒免疫，但我们发现独立于toll样受体9的信号通路在产生针对MCMV的免疫应答中很重要，包括干扰素α的产生和NK细胞毒性的诱导。值得注意的是，MCMV激活的CD11b(+) dc过继转移改善了MCMV感染的控制，表明这些细胞在体内参与控制病毒复制。
Dendritic cells (DCs) regulate various aspects of innate immunity, including natural killer (NK) cell function. Here we define the mechanisms involved in DC - NK cell interactions during viral infection. NK cells were efficiently activated by murine cytomegalovirus ( MCMV) - infected CD11b(+) DCs. NK cell cytotoxicity required interferon-alpha and interactions between the NKG2D activating receptor and NKG2D ligand, whereas the production of interferon-gamma by NK cells relied mainly on DC-derived interleukin 18. Although Toll-like receptor 9 contributes to antiviral immunity, we found that signaling pathways independent of Toll-like receptor 9 were important in generating immune responses to MCMV, including the production of interferon-alpha and the induction of NK cell cytotoxicity. Notably, adoptive transfer of MCMV-activated CD11b(+) DCs resulted in improved control of MCMV infection, indicating that these cells participate in controlling viral replication in vivo.