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首页> 外文期刊>The Journal of Immunology: Official Journal of the American Association of Immunologists >4-1BB Regulates Effector CD8 T Cell Accumulation in the Lung Tissue through a TRAF1-, mTOR-, and Antigen-Dependent Mechanism to Enhance Tissue-Resident Memory T Cell Formation during Respiratory Influenza Infection
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4-1BB Regulates Effector CD8 T Cell Accumulation in the Lung Tissue through a TRAF1-, mTOR-, and Antigen-Dependent Mechanism to Enhance Tissue-Resident Memory T Cell Formation during Respiratory Influenza Infection

机译：4-1BB通过TRAF1，MTOR-和抗原依赖性机制调节肺组织中的效应CD8 T细胞积累，以增强呼吸流感感染期间的组织居民记忆T细胞形成

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摘要

The TNFR superfamily member 4-1BB is important in the establishment of tissue-resident memory T cells (Trm) in the lung tissue following influenza infection. Moreover, supraphysiological boosting of 4-1BB in the airways during the boost phase of a prime-boost immunization regimen increases the long-lived Trm population, correlating with increased protection against heterotypic challenge. However, little is known about how 4-1BB contributes to the establishment of the lung Trm population. In this study, we show that effects of 4-1BB on lung Trm accumulation are already apparent at the effector stage, suggesting that the major role of 4-1BB in Trm formation is to allow persistence of CD8 T effector cells in the lung as they transition to Trm. Using supraphysiological stimulation of 4-1BB in the boost phase of a prime-boost immunization, we show that the effect of 4-1BB on Trm generation requires local delivery of both Ag and costimulation, is inhibited by rapamycin treatment during secondary CD8 effector T cell expansion, and is dependent on the signaling adaptor TRAF1. The decrease in lung Trm following early rapamycin treatment is accompanied by increased circulating memory T cells, as well as fewer effectors, suggesting a role for mammalian target of rapamycin (mTOR) in the formation of Trm through effects on the accumulation of effector precursors. Taken together, these data point to an important role for 4-1BB, TRAF1, and mTOR in the persistence of CD8 effector T cells in the lung parenchyma, thereby allowing the transition to Trm.
机译：TNFR超家族成员4-1BB在流感感染后肺组织中的组织 - 驻留记忆T细胞（TRM）是重要的。此外，在促进免疫制剂的增压阶段期间，气道中4-1BB的超级性升压增加了长期的TRM群，与抗异型挑战的保护。然而，关于4-1BB如何为肺部TRM人口建立的贡献少而闻名。在这项研究中，我们表明，4-1BB对肺部TRM积累的影响在效应阶段已经显而易见，表明4-1BB在TRM形成中的主要作用是允许肺活量的肺活量过渡到TRM。在素增压免疫的增压阶段使用求解阶段，表明4-1BB对TRM的效果需要局部递送AG和刺激，在次级CD8效应T细胞期间受雷帕霉素治疗抑制扩展，并取决于信令适配器TRAF1。早期雷帕霉素治疗后的肺部TRM的减少伴随着增加的循环记忆T细胞，以及较少的效果，表明哺乳动物催留催化剂（MTOR）的作用，通过对效应前体的积累产生TRM的形成。在一起，这些数据指向4-1BB，TRAF1和MTOR在肺实质中CD8效应T细胞的持续存在的重要作用，从而允许过渡到TRM。

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