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首页> 外文期刊>Vaccine >A West Nile virus NS4B-P38G mutant strain induces adaptive immunity via TLR7-MyD88-dependent and independent signaling pathways
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A West Nile virus NS4B-P38G mutant strain induces adaptive immunity via TLR7-MyD88-dependent and independent signaling pathways

机译：西尼罗河病毒NS4B-P38G突变株通过TLR7-MyD88依赖和独立的信号传导途径诱导适应性免疫

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Prior work shows that an attenuated West Nile virus (WNV), the nonstructural (NS)4B-P38G mutant infection in mice induced strong immune responses and protected host from subsequent lethal wildtype WNV infection. Here, we investigated NS4B-P38G mutant infection in myeloid differentiation factor 88-deficient (MyD88(-/-)) and Toll-like receptor 7-deficient (TLR7(-/-)) mice and found they had enhanced susceptibility compared to wild-type mice. Both groups had lower WNV-specific IgM response and reduced effector T cell functions. Dendritic cells (DCs) also exhibited a reduced maturation and impaired antigen-presenting functions compared to wild-type DCs. Moreover, infection with NS4B-P38G mutant in TLR7(-/-) and MyD88(-/-) mice provided full and partial protection respectively from subsequent challenge with lethal wild-type WNV. There were reduced T cell responses in MyD88(-/-) and interleukin-1 receptor deficient (IL-1R(-/-)) mice during secondary challenge with wild-type WNV. In contrast, TLR7(-/-) mice displayed normal T cell functions. Collectively, these results suggest that TLR7-dependent MyD88 signaling is required for T cell priming during NS4B-P38G mutant infection, whereas the TLR7-independent MyD88 signaling pathways are involved in memory T cell development, which may contribute to host protection during secondary challenge with wild-type WNV
机译：先前的工作表明，小鼠中的减毒西尼罗河病毒（WNV），非结构性（NS）4B-P38G突变体感染可诱导强烈的免疫反应，并保护宿主免受随后的致命性野生型WNV感染。在这里，我们调查了髓样分化因子88缺陷（MyD88（-/-））和Toll样受体7缺陷（TLR7（-/-））小鼠的NS4B-P38G突变体感染，发现它们与野生动物相比具有更高的易感性型小鼠。两组均具有较低的WNV特异性IgM反应和降低的效应T细胞功能。与野生型DC相比，树突状细胞（DC）的成熟度降低，抗原呈递功能受损。而且，在TLR7（-/-）和MyD88（-/-）小鼠中感染NS4B-P38G突变体分别提供了全部和部分保护，使其免受随后用致死性野生型WNV攻击。在野生型WNV的第二次攻击期间，MyD88（-/-）和白细胞介素1受体缺陷（IL-1R（-/-））小鼠的T细胞应答降低。相比之下，TLR7（-/-）小鼠显示正常的T细胞功能。总的来说，这些结果表明NS4B-P38G突变体感染期间T细胞启动需要TLR7依赖的MyD88信号传导，而记忆T细胞发育涉及TLR7无关的MyD88信号传导途径，这可能有助于继发性攻击期间宿主的保护野生型WNV

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