The diversity of myeloid immune cells shaping wound repair and fibrosis in the lung.

In healthy circumstances the immune system coordinates tissue repair responses in a tight balance that entails efficient inflammation for removal of potential threats, proper wound closure, and regeneration to regain tissue function. Pathological conditions, continuous exposure to noxious agents, and even ageing can dysregulate immune responses after injury. This dysregulation can lead to a chronic repair mechanism known as fibrosis. Alterations in wound healing can occur in many organs, but our focus lies with the lung as it requires highly regulated immune and repair responses with its continuous exposure to airborne threats. Dysregulated repair responses can lead to pulmonary fibrosis but the exact reason for its development is often not known. Here, we review the diversity of innate immune cells of myeloid origin that are involved in tissue repair and we illustrate how these cell types can contribute to the development of pulmonary fibrosis. Moreover, we briefly discuss the effect of age on innate immune responses and therefore on wound healing and we conclude with the implications of current knowledge on the avenues for future research.

在健康的情况下，免疫系统以一种紧密的平衡协调组织修复反应，这需要有效的炎症来清除潜在威胁、恰当的伤口闭合以及再生以恢复组织功能。病理状况、持续接触有害物质，甚至衰老都可能使受伤后的免疫反应失调。这种失调会导致一种被称为纤维化的慢性修复机制。伤口愈合的改变可发生在许多器官，但我们关注的是肺，因为它持续暴露于空气中的威胁，需要高度调节的免疫和修复反应。失调的修复反应可导致肺纤维化，但其发生的确切原因往往不清楚。在此，我们综述了参与组织修复的髓系固有免疫细胞的多样性，并阐明了这些细胞类型如何促进肺纤维化的发展。此外，我们简要讨论了年龄对固有免疫反应的影响，进而对伤口愈合的影响，并以当前知识对未来研究途径的启示作为结论。