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Bystander Activation of Pulmonary Trm Cells Attenuates the Severity of Bacterial Pneumonia by Enhancing Neutrophil Recruitment.
Cell Reports ( IF 7.5 ) Pub Date : 2019-12-24 , DOI: 10.1016/j.celrep.2019.11.103
Chenghao Ge 1 , Ian R Monk 2 , Angela Pizzolla 2 , Nancy Wang 2 , James G Bedford 2 , Timothy P Stinear 2 , Glen P Westall 3 , Linda M Wakim 2
Affiliation  

Tissue-resident memory T (Trm) cells are described as having a "sensing and alarming" function, meaning they can rapidly release cytokines in response to local cognate antigen recognition, which in turn, draws circulating immune cells into the tissue. Here, we show noncognate, bystander activation can also trigger the sensing and alarming function of pulmonary CD8+ Trm cells. Virus-specific CD8+ Trm cells lodged in the lung parenchyma, but not memory CD8+ T cells located in the vasculature, rapidly synthesize interferon γ (IFN-γ) following the inhalation of heat-killed bacteria or bacterial products, a process driven by interleukin-12 (IL-12)/IL-18 exposure. We show that a respiratory bacterial infection leads to bystander activation of lung Trm cells that boosts neutrophil recruitment into the airways and attenuates the severity of bacterial pneumonia. These data reveal that lung Trm cells have innate-like properties, enabling amplification of inflammation and participation in noncognate responses to bacterial infections.

中文翻译:

肺Trm细胞的旁观者激活可通过增强中性粒细胞的吸收来减轻细菌性肺炎的严重程度。

组织驻留记忆T(Trm)细胞被描述为具有“传感和警报”功能,这意味着它们可以响应于局部同源抗原识别而快速释放细胞因子,从而将循环免疫细胞吸引到组织中。在这里,我们显示了非同源的旁观者激活也可以触发肺CD8 + Trm细胞的感知和警报功能。吸入热杀死细菌或细菌产物后,病毒特异性CD8 + Trm细胞驻留在肺实质中,而不是记忆在脉管系统中的记忆CD8 + T细胞迅速合成干扰素γ(IFN-γ),这一过程由白介素- 12(IL-12)/ IL-18曝光。我们表明,呼吸道细菌感染会导致肺Trm细胞的旁观者激活,从而增强嗜中性白细胞向气道的募集并减轻细菌性肺炎的严重性。这些数据表明,肺Trm细胞具有先天性特性,能够放大炎症反应并参与对细菌感染的非同源反应。
更新日期:2019-12-25
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