Toll-like receptors activate innate and adaptive immunity by using dendritic cell-intrinsic and -extrinsic mechanisms.
Toll-like receptors activate innate and adaptive immunity by using dendritic cell-intrinsic and -extrinsic mechanisms.
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DOI：
10.1016/j.immuni.2008.05.016
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发表时间：
2008-08-15
期刊：
影响因子：
32.4
通讯作者：
DeFranco, Anthony L.
中科院分区：
文献类型：
--
作者：
Hou, Baidong;Reizis, Boris;DeFranco, Anthony L.
Toll样受体在启动感染获得性免疫反应中发挥重要作用，但其在体内特定细胞类型中的作用尚未确定。在这里，我们报告了在树突状细胞(DC)中选择性地缺乏关键的TLR信号适配器MyD88的小鼠的生成。在这些小鼠中，早期炎性细胞因子的产生，特别是IL-12，在TLR刺激后显著减少。然而，自然杀伤细胞和自然杀伤T细胞的天然干扰素γ反应和抗原特异性CD4T细胞的TH1极化在用可溶性TLR9L处理后严重受损，但在给予聚集的TLR9L后基本完好无损。这些结果表明，TLR配体的物理形式影响哪些细胞可以对其做出反应，DC和其他先天免疫细胞可以通过TLRs做出反应，并协同促进TH1对聚集刺激的适应性免疫反应。
Toll-like receptors (TLRs) play prominent roles in initiating adaptive immune responses to infection, but their roles in particular cell types in vivo are not established. Here we report the generation of mice selectively lacking the crucial TLR-signaling adaptor MyD88 in dendritic cells (DCs). In these mice, the early production of inflammatory cytokines, especially IL-12, was substantially reduced following TLR stimulation. Whereas, the innate interferon γ response of natural killer cells and natural killer T cells, and TH1 polarization of antigen-specific CD4 T cells were severely compromised after treatment with a soluble TLR9 ligand, they were largely intact following administration of an aggregated TLR9 ligand. These results demonstrate that the physical form of a TLR ligand affects which cells can respond to it and that DCs and other innate immune cells can respond via TLRs and collaborate in promoting TH1 adaptive immune responses to an aggregated stimulus.
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影响因子：
32.4
作者：
Jung, S;Unutmaz, D;Lang, RA
通讯作者：
Lang, RA
DOI：
10.1084/jem.20062648
发表时间：
2007-07-09
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Caton ML;Smith-Raska MR;Reizis B
通讯作者：
Reizis B
影响因子：
56.9
作者：
MULLER, U;STEINHOFF, U;AGUET, M
通讯作者：
AGUET, M
影响因子：
64.8
作者：
Honda, K;Ohba, Y;Taniguchi, T
通讯作者：
Taniguchi, T
影响因子：
2.2
作者：
AIDA, Y;PABST, MJ
通讯作者：
PABST, MJ