Regulating the adaptive immune response to respiratory virus infection.
Regulating the adaptive immune response to respiratory virus infection.
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DOI：
10.1038/nri3166
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发表时间：
2012-03-09
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影响因子：
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呼吸道是病毒进入人体的主要入口。如果感染严重，呼吸道感染会对肺部造成危及生命的损害。呼吸道已经进化出多种控制病毒复制以及限制免疫介导的炎症和组织损伤的策略。
肺间质内以及气道上皮细胞之间的多种固有免疫细胞类型，特别是树突状细胞（DCs），处于能够识别和采集气道颗粒（如病毒）的战略位置。
在呼吸道病毒感染的反应中，几个不同的树突状细胞亚群受到刺激，从肺部感染部位迁移到引流淋巴结。在这里，这些迁移的树突状细胞在启动针对入侵病毒的抗病毒适应性免疫反应中起着至关重要的作用。
进入受感染的肺部后，在淋巴结中产生的效应T细胞会根据炎症环境进行进一步的修饰。
效应T细胞与受感染肺部中呈现病毒抗原的各种细胞类型之间的共刺激受体 - 配体相互作用在原位调节宿主的适应性免疫反应。
产生促炎介质的效应T细胞也是调节性（抗炎）细胞因子的主要产生者，为效应T细胞在发炎组织中对病毒的反应提供了一种自我控制的微调机制。
控制病毒感染肺部中病毒复制和/或过度炎症的免疫机制也可能使从病毒感染中恢复的个体容易发生细菌重复感染。治疗策略应考虑平衡抑制病毒复制和过度炎症的需求与优化固有免疫吞噬细胞抗菌功能的需求，固有免疫吞噬细胞对于清除肺部细菌至关重要。
本文的网络版（doi:10.1038/nri3166）包含补充材料，授权用户可获取。
本文综述了固有免疫细胞和适应性免疫细胞在下呼吸道病毒感染反应中的相互作用，并描述了控制肺部抗病毒T细胞但也可能使个体易患后续肺部细菌感染的微调机制。
本文的网络版（doi:10.1038/nri3166）包含补充材料，授权用户可获取。
近年来，我们对下呼吸道病毒感染（包括流感病毒感染）的免疫理解有了一些进展。在这里，我们综述了病毒的细胞靶点以及肺部特有的宿主免疫反应特征。我们描述了固有免疫细胞和适应性免疫细胞在抗病毒免疫的诱导、表达和控制中的相互作用，并讨论了受感染的肺部环境对塑造抗病毒效应T细胞反应的影响。还讨论了关于呼吸道病毒感染后严重肺部细菌感染频率增加的机制的最新研究结果。
本文的网络版（doi:10.1038/nri3166）包含补充材料，授权用户可获取。
The respiratory tract is a major portal of entry for viruses into the body. Infection of the respiratory tract can, if severe, induce life-threatening damage to the lungs. Various strategies to control virus replication and to limit immune-mediated inflammation and tissue injury have evolved in the respiratory tract. Multiple innate immune cell types, particularly dendritic cells (DCs), within the pulmonary interstitium and between airway epithelial cells are strategically poised to recognize and sample airway particulates, such as viruses. In response to respiratory virus infection, several distinct DC subsets are stimulated to migrate from the site of infection in the lungs to the draining lymph nodes. Here, these migrant DCs have a crucial role in initiating the antivirus adaptive immune response to the invading viruses. After entering the infected lungs, effector T cells that were generated in the lymph nodes undergo further modifications that are shaped by the inflammatory milieu. Co-stimulatory receptor–ligand interactions between effector T cells and various cell types presenting viral antigens in the infected lungs modulate the host adaptive immune response in situ. Effector T cells that produce pro-inflammatory mediators are also the major producers of regulatory (anti-inflammatory) cytokines, providing a fine-tuning mechanism of self-control by effector T cells responding to viruses in the inflamed tissue. The immune mechanisms that control virus replication and/or excessive inflammation in the virus-infected lungs can also predispose the individual recovering from a virus infection to bacterial superinfection. Therapeutic strategies should consider balancing the need to inhibit virus replication and excessive inflammation with the need to optimize the antibacterial functions of innate immune phagocytes, which are crucial for clearing the bacteria from the lungs. The online version of this article (doi:10.1038/nri3166) contains supplementary material, which is available to authorized users. This article reviews the interplay between innate and adaptive immune cells in the response to viral infection of the lower respiratory tract and describes the fine-tuning mechanisms that control antiviral T cells in the lungs but that can also predispose an individual to subsequent pulmonary bacterial infections. The online version of this article (doi:10.1038/nri3166) contains supplementary material, which is available to authorized users. Recent years have seen several advances in our understanding of immunity to virus infection of the lower respiratory tract, including to influenza virus infection. Here, we review the cellular targets of viruses and the features of the host immune response that are unique to the lungs. We describe the interplay between innate and adaptive immune cells in the induction, expression and control of antiviral immunity, and discuss the impact of the infected lung milieu on moulding the response of antiviral effector T cells. Recent findings on the mechanisms that underlie the increased frequency of severe pulmonary bacterial infections following respiratory virus infection are also discussed. The online version of this article (doi:10.1038/nri3166) contains supplementary material, which is available to authorized users.
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