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首页> 外文期刊>Infection and immunity >CD8+-T-Cell Response to Secreted and Nonsecreted Antigens Delivered by Recombinant Listeria monocytogenes during Secondary Infection
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CD8+-T-Cell Response to Secreted and Nonsecreted Antigens Delivered by Recombinant Listeria monocytogenes during Secondary Infection

机译：CD8 + -T细胞对二次感染期间重组李斯特菌重组李斯特菌传递的分泌和非分泌抗原的反应。

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Understanding how existing antivector immunity impacts live vaccine delivery systems is critical when the same vector system may be used to deliver different antigens. We addressed the impact of antivector immunity, elicited by immunization with attenuated actA-deficient Listeria monocytogenes, on the CD8+-T-cell response to a well-characterized lymphocytic choriomeningitis virus epitope, NP118-126, delivered by infection with recombinant L. monocytogenes. Challenges of immune mice with actA-deficient and with wild-type recombinant L. monocytogenes generated similar numbers of CD8+ T cells specific for the NP118-126 epitope. High-dose immunization with actA-deficient L. monocytogenes resulted in substantial numbers of CD8+ T cells specific for the L. monocytogenes LLO91-99 epitope in the effector and memory stages of the T-cell response. Challenge of these immune mice with recombinant L. monocytogenes resulted in rapid control of the infection and decreased CD8+-T-cell responses against both the secreted and nonsecreted form of the recombinant antigen compared to the response of na?ve mice. In contrast, mice immunized with a low dose of actA-deficient L. monocytogenes had ～10-fold fewer effector and memory T cells specific for LLO91-99 and a substantially higher CD8+-T-cell response against the recombinant antigen after challenge with recombinant L. monocytogenes. Although mice immunized with low-dose actA-deficient L. monocytogenes had a substantial recall response to LLO91-99, which reached the same levels by 5 to 7 days postchallenge as that in high-dose-immunized mice, they exhibited decreased ability to control L. monocytogenes replication. Thus, the level of antivector immunity impacts the control of infection and efficiency of priming responses against new antigens introduced with the same vector.
机译：当可以使用相同的载体系统递送不同的抗原时，了解现有抗载体免疫如何影响活疫苗递送系统至关重要。我们研究了抗载体免疫的影响，该抗免疫是通过对减弱的 actA 缺陷型单核细胞增生李斯特菌免疫引起的，对CD8 + -T细胞应答一种特征明确的淋巴细胞脉络膜脑膜炎病毒抗原表位NP118-126，通过感染重组体 L传递。单核细胞增生。缺乏 actA 和野生型重组 L的免疫小鼠的挑战。单核细胞增生产生的NP118-126表位特异性CD8 + T细胞数量相近。用 actA 缺陷的 L进行大剂量免疫。单核细胞增生导致大量的 L特异性CD8 + T细胞。单核细胞增生李斯特LLO91-99表位在T细胞反应的效应和记忆阶段。用重组 L攻击这些免疫小鼠。与幼稚小鼠的反应相比，单核细胞增生病能够快速控制感染并降低针对分泌型和非分泌型重组抗原的CD8 + -T细胞反应。相反，用低剂量的 actA 缺陷型 L免疫的小鼠。重组攻击后，单核细胞增生李斯特氏菌对LLO91-99特异的效应和记忆T细胞减少约10倍，对重组抗原的CD8 + -T细胞应答明显更高L.单核细胞增生。虽然小鼠用低剂量 actA 缺陷型 L免疫。单核细胞增生李斯特氏菌对LLO91-99的记忆力明显增强，在攻击后5至7天达到了与大剂量免疫小鼠相同的水平，其控制 L的能力下降。单核细胞增生复制。因此，抗载体免疫力的水平影响感染的控制和针对由相同载体引入的新抗原的引发反应的效率。

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