Center for Lung Biology, University of Washington, Seattle, Washington.
Department of Biochemistry, Faculty of Medicine, Universities of Giessen and Marburg Lung Center, Giessen, Germany.
J Histochem Cytochem. 2018 Apr;66(4):213-227. doi: 10.1369/0022155417740880. Epub 2018 Jan 1.
It is evident that components of the extracellular matrix (ECM) act as danger-associated molecular patterns (DAMPs) through direct interactions with pattern recognition receptors (PRRs) including Toll-like receptors (TLRs) and inflammasomes. Through these interactions, ECM-derived DAMPs autonomously trigger sterile inflammation or prolong pathogen-induced responses through the production of proinflammatory mediators and the recruitment of leukocytes to sites of injury and infection. Recent research, however, suggests that ECM-derived DAMPs are additionally involved in the resolution and fine-tuning of inflammation by orchestrating the production of anti-inflammatory mediators that are required for the resolution of tissue inflammation and the transition to acquired immunity. Thus, in this review, we discuss the current knowledge of the interplay between ECM-derived DAMPs and the innate immune signaling pathways that are activated to provide temporal control of innate immunity.
显然,细胞外基质(ECM)的成分通过与模式识别受体(PRRs)(包括 Toll 样受体(TLRs)和炎性体)的直接相互作用,充当危险相关分子模式(DAMPs)。通过这些相互作用,ECM 来源的 DAMPs 通过产生促炎介质和招募白细胞到损伤和感染部位,自主触发无菌性炎症或延长病原体诱导的反应。然而,最近的研究表明,ECM 来源的 DAMPs 还通过协调产生抗炎介质来参与炎症的消退和微调,这些介质是组织炎症消退和获得性免疫过渡所必需的。因此,在这篇综述中,我们讨论了 ECM 来源的 DAMPs 与先天免疫信号通路之间相互作用的最新知识,这些信号通路被激活以提供对先天免疫的时间控制。