Type I interferons regulate cytolytic activity of memory CD8(+) T cells in the lung airways during respiratory virus challenge.
Type I interferons regulate cytolytic activity of memory CD8(+) T cells in the lung airways during respiratory virus challenge.
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DOI：
10.1016/j.immuni.2010.06.016
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发表时间：
2010-07-23
期刊：
影响因子：
32.4
通讯作者：
Woodland DL
中科院分区：
文献类型：
--
作者：
Kohlmeier JE;Cookenham T;Roberts AD;Miller SC;Woodland DL
肺气道中的记忆性CD8+ T细胞通过限制早期病毒复制提供了对继发性呼吸道病毒攻击的保护。在这里，我们证明了尽管气道驻留的记忆性CD8+ T细胞的细胞溶解能力较差，但在回忆反应中早期募集到气道的记忆性CD8+ T细胞的细胞溶解能力显著增强。这种增强的裂解活性不需要同源抗原刺激，而是依赖于通过干扰素-α受体（Ifnar1）的STAT1转录因子信号传导，导致颗粒酶B蛋白在小鼠和人类病毒特异性T细胞中不依赖抗原表达。通过Ifnar1的信号传导是增强肺气道中记忆性CD8+ T细胞的裂解活性和控制早期病毒复制所必需的。这些发现表明，先天炎症信号直接作用于记忆T细胞，使它们能够在进入感染组织后迅速摧毁被感染的宿主细胞。
Memory CD8+ T cells in the lung airways provide protection from secondary respiratory virus challenge by limiting early viral replication. Here, we demonstrate that although airway-resident memory CD8+ T cells were poorly cytolytic, memory CD8+ T cells recruited to the airways early during a recall response showed markedly enhanced cytolytic ability. This enhanced lytic activity did not require cognate antigen stimulation, but rather was dependent on STAT1 transcription factor signaling through the interferon-α receptor (Ifnar1), resulting in the antigen-independent expression of granzyme B protein in both murine and human virus-specific T cells. Signaling through Ifnar1 was required for the enhanced lytic activity and control of early viral replication by memory CD8+ T cells in the lung airways. These findings demonstrate that innate inflammatory signals act directly on memory T cells, enabling them to rapidly destroy infected host cells once they enter infected tissues.
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影响因子：
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作者：
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影响因子：
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