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Danger-Associated Molecular Patterns Derived From the Extracellular Matrix Provide Temporal Control of Innate Immunity

机译:源自细胞外基质的危险相关分子模式提供了对先天性免疫的时间控制

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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.
机译:显然,细胞外基质(ECM)的成分通过与包括Toll样受体(TLR)和炎症小体的模式识别受体(PRR)的直接相互作用,充当了与危险相关的分子模式(DAMP)。通过这些相互作用,ECM衍生的DAMP通过产生促炎性介质以及将白细胞募集到损伤和感染部位,自主触发无菌炎症或延长病原体诱导的反应。但是,最近的研究表明,ECM衍生的DAMPs还通过协调产生消炎介质的生产来参与炎症的解决和微调,这些消炎介质是解决组织炎症和过渡到获得性免疫所必需的。因此,在这篇综述中,我们讨论了ECM衍生的DAMP与先天免疫信号通路之间相互作用的当前知识,先天免疫信号通路被激活以提供先天免疫的时间控制。

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