Lung fibrosis is characterised by the accumulation of extracellular matrix within the lung and is secondary to both known and unknown aetiologies. This accumulation of scar tissue limits gas exchange causing respiratory insufficiency. The pathogenesis of lung fibrosis is poorly understood, but immunologic-based treatments have been largely ineffective. Despite this, accumulating evidence suggests that innate immune cells and receptors play important modulatory roles in the initiation and propagation of the disease. Paradoxically, while innate immune signalling may be important for the pathogenesis of fibrosis, there is also evidence to suggest that innate immune function against pathogens may be impaired, leading to dysregulated and/or impaired host defence. This review summarises the evidence for this pathologic two-way street, highlights new concepts of pathogenesis and recommends future directions for research emphasis.

中文翻译：

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一条病态的两条路：先天免疫如何影响肺纤维化，而纤维化如何影响肺免疫。

肺纤维化的特征在于肺内细胞外基质的积累，继发于已知和未知的病因。这种疤痕组织的积累限制了气体交换，导致呼吸功能不全。肺纤维化的发病机制知之甚少，但基于免疫学的治疗在很大程度上是无效的。尽管如此，越来越多的证据表明，先天免疫细胞和受体在疾病的发生和传播中起着重要的调节作用。矛盾的是，虽然先天免疫信号可能对纤维化的发病机制很重要，但也有证据表明，针对病原体的先天免疫功能可能受损，导致宿主防御失调和/或受损。这篇综述总结了这条病态双向街道的证据，