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

譯文

慢性Mtb感染期間免疫病理學(xué)調(diào)控為宿主存活所必需。免疫病理學(xué)在肺部Mtb感染具有重要作用，那么IL-17與Th17細(xì)胞很可能具有一定作用。其作用很有可能受到嗜中性粒細(xì)胞的介導(dǎo)。

如前所述，嗜中性粒細(xì)胞招募與存活可能為IL-17促進(jìn)肉芽腫形成的一個機(jī)制。但是，此種應(yīng)答需要一定的調(diào)控。這是因?yàn)榉尾看罅渴戎行粤＜?xì)胞的積累與預(yù)后欠佳、肺部病理變化增加相關(guān)。 實(shí)際上，遺傳易感性小鼠內(nèi)常出現(xiàn)嗜中性粒細(xì)胞積累。人類臨床研究表明，TB患者主要受感染的細(xì)胞為嗜中性粒細(xì)胞。表明這些細(xì)胞可以為細(xì)菌復(fù)制提供適當(dāng)?shù)臈l件。有趣的是，血液嗜中性粒細(xì)胞轉(zhuǎn)錄信號需要I型IFN-αβ的激活。而γ-干擾素存在于活性感染期，潛伏期并未發(fā)現(xiàn)該干擾素的存在。這些數(shù)據(jù)闡述了TB發(fā)病過程中嗜中性粒細(xì)胞的表型。此外，嗜中性粒細(xì)胞暴露于IL-17或IL-23可影響這些細(xì)胞的穩(wěn)態(tài)及表型，以至于發(fā)生免疫學(xué)病變。IL-17可能通過嗜中性粒細(xì)胞招募及促進(jìn)特定炎癥趨化因子分泌對機(jī)體產(chǎn)生有益影響。但是大量暴露于IL-17或IL-23可延長細(xì)胞存活期，改變細(xì)胞表型，并導(dǎo)致免疫病理學(xué)變化。