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ISSN 打印: 1040-8401
ISSN 在线: 2162-6472

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DOI: 10.1615/CritRevImmunol.2018026611
pages 367-378

Manning the Barricades: Lung Fibroblasts and CD4+ T Cells as the Last Line of Defense against Bacterial Invasion?

Andrew J. Hutton
Clinical and Experimental Sciences, University of Southampton Faculty of Medicine, Sir Henry Wellcome Laboratories, Southampton General Hospital, Southampton, United Kingdom
Jane A. Warner
Clinical and Experimental Sciences, University of Southampton Faculty of Medicine, Sir Henry Wellcome Laboratories, Southampton General Hospital, Southampton, United Kingdom
Karl J. Staples
Clinical and Experimental Sciences, University of Southampton Faculty of Medicine, Sir Henry Wellcome Laboratories, Southampton General Hospital, Southampton, United Kingdom; Wessex Investigational Sciences Hub, University of Southampton Faculty of Medicine, Southampton General Hospital, Southampton, United Kingdom

ABSTRACT

Fibroblasts are a major structural cell in the human lung, being responsible for the production of extracellular matrix components that provide the intricate structure necessary for correct lung function. Generally located in the submucosa, fibroblasts do not usually directly interact with the commensal microbes that we now know are resident in the airways. However, during situations in which alveolar macrophages and epithelial cells are impaired, for example, during severe viral infections leading to pneumonia, bacteria can invade the lung mesenchyme. In these circumstances, fibroblasts may represent another immunological barrier to bacterial invasion, not just as innate immune effectors, but also by interacting with migrating and tissue-resident adaptive immune cell populations, such as CD4+ T cells. The cytokines produced by CD4+ T helper cells are integral in directing appropriate innate and adaptive immune responses against bacteria, but the nature of fibroblast-CD4+ cell interaction, unlike the CD8+ T-cell interaction, is not clearly established. Here, we review the responses of lung fibroblasts to bacteria and discuss emerging data indicating a key role for these cells in directly presenting bacterial antigens to CD4+ T cells.


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