Danger-Associated Molecular Patterns Derived From the Extracellular Matrix Provide Temporal Control of Innate Immunity
2018/01/01 by Charles W. Frevert, Jessica L Felgenhauer, Jessica Felgenhauer +4 · 26 citations
Immunology and Microbiology · Biochemistry, Genetics and Molecular Biology · #Immune Response and Inflammation #Inflammasome and immune disorders #Neutrophil, Myeloperoxidase and Oxidative Mechanisms
paper · pdf · doi:10.1369/0022155417740880
Abstract
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.
Cited by
- Biglycan is a new high-affinity ligand for CD14 in macrophages
- Generation of a multi-functional, target organ-specific, anti-fibrotic molecule by molecular engineering of the extracellular matrix protein, decorin. [europepmc]
- Hyaluronan, Cancer-Associated Fibroblasts and the Tumor Microenvironment in Malignant Progression. [europepmc]
- Hyaluronan biology: A complex balancing act of structure, function, location and context. [europepmc]
- Proteoglycans and Immunobiology of Cancer-Therapeutic Implications. [europepmc]
- Cellular and Molecular Mechanisms in the Pathogenesis of Classical, Vascular, and Hypermobile Ehlers‒Danlos Syndromes. [europepmc]
- Activation of Myd88-Dependent TLRs Mediates Local and Systemic Inflammation in a Mouse Model of Primary Sjögren's Syndrome. [europepmc]
- Current Approaches Targeting the Wound Healing Phases to Attenuate Fibrosis and Scarring. [europepmc]
- CCN1 is an opsonin for bacterial clearance and a direct activator of Toll-like receptor signaling. [europepmc]
- Chronic Hypersensitivity Pneumonitis, an Interstitial Lung Disease with Distinct Molecular Signatures. [europepmc]
- Adipocyte-Derived Versican and Macrophage-Derived Biglycan Control Adipose Tissue Inflammation in Obesity. [europepmc]
- Increased immunosuppression impairs tissue homeostasis with aging and age-related diseases. [europepmc]
- Concepts of extracellular matrix remodelling in tumour progression and metastasis. [europepmc]
- Regulation of cellular senescence by extracellular matrix during chronic fibrotic diseases. [europepmc]
- The Long Non-coding RNAs: Paramount Regulators of the NLRP3 Inflammasome. [europepmc]
- Danger-Sensing/Patten Recognition Receptors and Neuroinflammation in Alzheimer's Disease. [europepmc]
- Immunomodulatory Role of the Extracellular Matrix Within the Liver Disease Microenvironment. [europepmc]
- Lyme Disease Pathogenesis. [europepmc]
- The Damage-Associated Molecular Patterns (DAMPs) as Potential Targets to Treat Osteoarthritis: Perspectives From a Review of the Literature. [europepmc]
- Control of innate immune response by biomaterial surface topography, energy, and stiffness. [europepmc]
- Matrix lumican endocytosed by immune cells controls receptor ligand trafficking to promote TLR4 and restrict TLR9 in sepsis. [europepmc]
- Fibroblasts: Origins, definitions, and functions in health and disease. [europepmc]
- Fibroblast Memory in Development, Homeostasis and Disease. [europepmc]
- Damage-Associated Molecular Patterns (DAMPs) in Retinal Disorders. [europepmc]
- Rationale for sequential extracorporeal therapy (SET) in sepsis. [europepmc]
- Repair of the Infarcted Heart: Cellular Effectors, Molecular Mechanisms and Therapeutic Opportunities. [europepmc]
Related