免疫病理学翻译

原文
Regulation of immunopathology during chronic Mtb infection is essential for host survival. As immunopathology is a central feature of Mtb lung infection, it is not surprising that IL-17 and Th17 cells have a role to play. Importantly, this role also seems to be mediated, at least in part, by neutrophils.
As discussed earlier, neutrophil recruitment and survival may be one of the mechanisms by which IL-17 promotes granuloma organization. However, this response needs regulation since the accumulation of large numbers of neutrophils in the lung is generally associated with a bad prognosis and increased lung pathology. Indeed, neutrophil accumulation is common in genetically susceptible mice. In humans, it has been shown that neutrophils are the predominant infected cell types in active TB patients, suggesting that these cells provide a permissive environment for bacillary replication. Interestingly, it was recently shown that a transcriptional signature in blood neutrophils, indicating activation of these cells with type I IFN-ab and IFN-g is present in patients with active as opposed to latent TB. These data implicate the phenotype of neutrophils in the pathogenesis of TB. In line with these data it has also been shown that, exposure of neutrophils to IL-17 or IL-23 can change the homeostasis and phenotype of these cells making them more prone to cause immunopathology. In other words, IL-17 may have beneficial effects early on, by recruiting neutrophils and promote secretion of tissue-specific homing chemokines, but extensive exposure of neutrophils to IL-17 or IL-23 can make these cells survive longer, change their phenotype and cause immunopathology

译文

慢性Mtb感染期间免疫病理学调控为宿主存活所必需。免疫病理学在肺部Mtb感染具有重要作用，那么IL-17与Th17细胞很可能具有一定作用。其作用很有可能受到嗜中性粒细胞的介导。

如前所述，嗜中性粒细胞招募与存活可能为IL-17促进肉芽肿形成的一个机制。但是，此种应答需要一定的调控。这是因为肺部大量嗜中性粒细胞的积累与预后欠佳、肺部病理变化增加相关。 实际上，遗传易感性小鼠内常出现嗜中性粒细胞积累。人类临床研究表明，TB患者主要受感染的细胞为嗜中性粒细胞。表明这些细胞可以为细菌复制提供适当的条件。有趣的是，血液嗜中性粒细胞转录信号需要I型IFN-αβ的激活。而γ-干扰素存在于活性感染期，潜伏期并未发现该干扰素的存在。这些数据阐述了TB发病过程中嗜中性粒细胞的表型。此外，嗜中性粒细胞暴露于IL-17或IL-23可影响这些细胞的稳态及表型，以至于发生免疫学病变。IL-17可能通过嗜中性粒细胞招募及促进特定炎症趋化因子分泌对机体产生有益影响。但是大量暴露于IL-17或IL-23可延长细胞存活期，改变细胞表型，并导致免疫病理学变化。