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Abstract：
Following Mycobacterium tuberculosis infection, alveolar macrophages are initially infected but ineffectively restrict bacterial replication. The distribution of M. tuberculosis among different cell types in the lung changes with the onset of T cell immunity when the dominant infected cellular niche shifts from alveolar to monocyte-derived macrophages (MDM). We hypothesize that changes in bacterial distribution among different cell types is driven by differences in T cell recognition of infected cells and their subsequent activation of antimicrobial effector mechanisms. We show that CD4 and CD8 T cells efficiently eliminate M. tuberculosis infection in alveolar macrophages, but they have less impact on suppressing infection in MDM, which may be a bacterial niche. Importantly, CD4 T cell responses enhance MDM recruitment to the lung. Thus, the outcome of infection depends on the interaction between the T cell subset and the infected cell; both contribute to the resolution and persistence of the infection.
摘要：
结核分枝杆菌感染后，肺泡巨噬细胞最初被感染，但不能有效地限制细菌复制。当显性感染的细胞生态位从肺泡转移到单核细胞衍生的巨噬细胞（MDM）时，随着T细胞免疫的发生，结核分枝杆菌在肺中不同细胞类型中的分布也会发生变化。我们假设不同细胞类型之间细菌分布的变化是由感染细胞的T细胞识别差异及其随后的抗微生物效应机制激活驱动的。我们显示CD4和CD8T细胞有效消除肺泡巨噬细胞中的结核分枝杆菌感染，但是它们对抑制MDM感染的影响较小，可能是细菌生态位。重要的是,CD4T细胞应答增强MDM向肺的募集。因此，感染的结果取决于T细胞亚群和感染细胞之间的相互作用;两者都有助于感染的解决和持续。
