Plasmacytoid dendritic cell ablation impacts early interferon responses and antiviral NK and CD8(+) T cell accrual.
Plasmacytoid dendritic cell ablation impacts early interferon responses and antiviral NK and CD8(+) T cell accrual.
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DOI：
10.1016/j.immuni.2010.11.020
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发表时间：
2010-12-14
期刊：
影响因子：
32.4
通讯作者：
Colonna M
中科院分区：
文献类型：
--
作者：
Swiecki M;Gilfillan S;Vermi W;Wang Y;Colonna M
浆细胞样树突状细胞（pDC）介导I型干扰素（IFN-I）对通过Toll样受体7（TLR 7）或TLR 9信号传导途径识别的病毒的应答。然而，pDC如何通过先天性和适应性免疫细胞调节抗病毒应答尚不清楚。我们产生了白喉毒素受体转基因小鼠，通过施用白喉毒素来选择性地消耗pDC。用已知激活pDC的病毒攻击pDC耗尽的小鼠。在鼠巨细胞病毒（MCMV）感染中，pDC耗竭减少早期IFN-I产生并增加病毒负荷，促进表达MCMV特异性受体Ly 49 H的自然杀伤（NK）细胞的扩增。在水泡性口炎病毒（VSV）感染期间，pDC耗竭增强早期病毒复制并损害病毒特异性细胞毒性T淋巴细胞的存活和积累。我们得出结论，pDC介导早期抗病毒IFN-I应答，并以病毒依赖性方式影响病毒特异性NK或CD 8 + T细胞的增加。
Plasmacytoid dendritic cells (pDCs) mediate type I interferon (IFN-I) responses to viruses that are recognized through the Toll-like receptor 7 (TLR7) or TLR9 signaling pathway. However, it is unclear how pDCs regulate the antiviral responses via innate and adaptive immune cells. We generated diphtheria toxin receptor transgenic mice to selectively deplete pDCs by administration of diphtheria toxin. pDC-depleted mice were challenged with viruses known to activate pDCs. In murine cytomegalovirus (MCMV) infection, pDC depletion reduced early IFN-I production and augmented viral burden facilitating the expansion of natural killer (NK) cells expressing the MCMV-specific receptor Ly49H. During vesicular stomatitis virus (VSV) infection, pDC depletion enhanced early viral replication and impaired the survival and accumulation of virus-specific cytotoxic T lymphocytes. We conclude that pDCs mediate early antiviral IFN-I responses and influence the accrual of virus-specific NK or CD8+ T cells in a virus-dependent manner.
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