Nonspecific recruitment of memory CD8+ T cells to the lung airways during respiratory virus infections
Nonspecific recruitment of memory CD8+ T cells to the lung airways during respiratory virus infections
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DOI：
10.4049/jimmunol.170.3.1423
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发表时间：
2003-02-01
影响因子：
4.4
通讯作者：
Woodland, DL
中科院分区：
文献类型：
--
作者：
Ely, KH;Cauley, LS;Woodland, DL
以前的研究表明，异源病毒感染通过交叉反应和旁观者效应的组合，对次级淋巴器官中原有的记忆T细胞群产生显著影响。然而，异源病毒感染对周围部位的效应/记忆T细胞的影响还不是很清楚。在这项研究中，我们分析了异种流感病毒感染对存在于肺部呼吸道的仙台病毒特异性CD8(+)效应/记忆细胞的影响。数据显示，感染流感的小鼠呼吸道中仙台病毒核蛋白324-332/K-b特异性CD8(+)记忆T细胞的数量有一过性增加，在感染后第4天达到顶峰。气管内转移研究和5-溴-2‘-脱氧尿嘧啶核苷掺入表明，这种增加是由于静止的记忆细胞重新进入呼吸道。此外，数据显示，这些迁徙的记忆细胞与肺部呼吸道的常驻记忆T细胞在表型上是不同的。仙台病毒的二次(同源)感染也会导致类似的非增殖性仙台病毒核蛋白324-332/K-b特异性CD8(+)记忆T细胞的流入。综上所述，这些数据表明，炎症可以加速记忆T细胞向非淋巴组织的迁移，是呼吸道感染期间正常回忆反应的一部分。
Previous studies have shown that heterologous viral infections have a significant impact on pre-existing memory T cell populations in secondary lymphoid organs through a combination of cross-reactive and bystander effects. However, the impact of heterologous viral infections on effector/memory T cells in peripheral sites is not well understood. In this study, we have analyzed the impact of a heterologous influenza virus infection on Sendai virus-specific CD8(+) effector/memory cells present in the lung airways. The data show a transient increase in the numbers of Sendai virus nucleoprotein 324-332/K-b-specific CD8(+) memory T cells in the airways of the influenza-infected mice peaking around day 4 postinfection. Intratracheal transfer studies and 5-bromo-2'-deoxyuridine incorporation demonstrate that this increase is due to the recruitment of resting memory cells into the airways. In addition, the data show that these immigrating memory cells are phenotypically distinct from the resident memory T cells of the lung airways. A similar influx of nonproliferating Sendai virus nucleoprotein 324-332/K-b-specific CD8(+) memory T cells is also induced by a secondary (homologous) infection with Sendai virus. Together, these data suggest that inflammation can accelerate memory T cell migration to nonlymphoid tissues and is a part of the normal recall response during respiratory infections.