Ishikawa Genta, Liu Angela, Herzog Erica L
Section of Pulmonary, Critical Care and Sleep Medicine, Department of Internal Medicine, Yale School of Medicine, New Haven, CT, United States.
Department of Pathology, Yale School of Medicine, New Haven, CT, United States.
Front Mol Biosci. 2021 Aug 9;8:676569. doi: 10.3389/fmolb.2021.676569. eCollection 2021.
While epithelial-fibroblast interactions are viewed as the primary drivers of Idiopathic Pulmonary Fibrosis (IPF), evidence gleaned from animal modeling and human studies implicates innate immunity as well. To provide perspective on this topic, this review synthesizes the available data regarding the complex role of innate immunity in IPF. The role of substances present in the fibrotic microenvironment including pathogen associated molecular patterns (PAMPs) derived from invading or commensal microbes, and danger associated molecular patterns (DAMPs) derived from injured cells and tissues will be discussed along with the proposed contribution of innate immune populations such as macrophages, neutrophils, fibrocytes, myeloid suppressor cells, and innate lymphoid cells. Each component will be considered in the context of its relationship to environmental and genetic factors, disease outcomes, and potential therapies. We conclude with discussion of unanswered questions and opportunities for future study in this area.
虽然上皮细胞与成纤维细胞的相互作用被视为特发性肺纤维化（IPF）的主要驱动因素，但从动物模型和人体研究中获得的证据也表明先天免疫也与之相关。为了对这一主题提供见解，本综述综合了有关先天免疫在IPF中复杂作用的现有数据。将讨论纤维化微环境中存在的物质的作用，包括源自入侵或共生微生物的病原体相关分子模式（PAMP），以及源自受损细胞和组织的危险相关分子模式（DAMP），同时还将讨论先天免疫细胞群体如巨噬细胞、中性粒细胞、纤维细胞、髓系抑制细胞和先天淋巴细胞的潜在作用。将在与环境和遗传因素、疾病结局及潜在治疗方法的关系背景下考虑每个组成部分。我们最后讨论了该领域未解决的问题以及未来研究的机会。
