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RIG-I as a Therapeutic Target for Nucleic Acid Nanoparticles (NANPs)
Published in Peixuan Guo, Kirill A. Afonin, RNA Nanotechnology and Therapeutics, 2022
Pattern recognition receptors (PRRs) are critical for the identification of pathogen motifs, pathogen-associated molecular patterns (PAMPs) and endogenous host molecules, damage-associated molecular patterns (DAMPs) that are released from stressed cells. Toll-like receptors (TLRs), nucleotide-biding oligomerization domain (NOD)-like receptors, retinoic acid-inducible gene-I (RIG-I)-like receptors (RLRs), and DNA sensors are classes of PRRs (Barbalat, Ewald, Mouchess, & Barton, 2011; Desmet & Ishii, 2012; Wu & Chen, 2014). Recognition of PAMPs and DAMPs initiates the expression and release of immune mediators to recruit and activate immune cells. Additionally, PRR signaling stimulates expression of costimulatory molecules, antigen uptake, processing, and presentation via the major histocompatibility complex (MHC) that contribute to the generation of antigen-specific adaptive immune responses (Desmet & Ishii, 2012). Due to the role of PRRs in generating innate and adaptive immune responses, PRRs remain a promising therapeutic target.
Application of Carbon Nanotubes in Cancer Vaccines as Drug Delivery Tools
Published in Loutfy H. Madkour, Nanoparticle-Based Drug Delivery in Cancer Treatment, 2022
Appropriate activation of APCs is crucial for unlocking their full T cell stimulatory capacity [128]. Innate activation of APCs is mediated by pattern recognition receptors (PRRs) such as toll-like receptors (TLRs), C-type lectin receptors (CLRs), and NOD-like receptors (NLRs) [129,130]. These receptors recognize ligands associated with invading pathogens known as pathogen-associated molecular patterns (PAMPs). Naturally occurring PAMPs or their synthetic analogues have been widely explored in vaccine formulations as adjuvants with the aim to promote immunity induction [130,131]. In particular, synthetic TLR9 agonists in form of oligodeoxynucleotides (ODN) containing unmethylated deoxycytidine-deoxyguanosine dinucleotide (CpG) motifs have been included as adjuvant in many clinically investigated cancer vaccine formulations (Figure 9.7) [132,133].
Host Response to Biomaterials
Published in Claudio Migliaresi, Antonella Motta, Scaffolds for Tissue Engineering, 2014
Sangeetha Srinivasan, Julia E. Babensee
Acute inflammation is the first stage of inflammation, and it is characterized by the early and rapid tissue infiltration of polymorphonuclear (PMN) cells or neutrophils.9 Tissue-resident MOs and dendritic cells (DCs) at the injured site, initiate the early events of acute inflammation.3 These cells recognize pathogens and danger signals via pattern recognition receptors (PRRs). They also secrete molecular mediators specifically chemokines, which provide chemotactic signals for the migration of PMNs from flowing blood to the site of inflammatory insult and cytokines, which activate the endothelium to support this cell recruitment.10 Though recruited in large numbers, PMNs are fairly short-lived and generally undergo apoptosis within 24 hours of the inflammatory response. Their main role is to cleanse the injury site, phagocytosing cellular and tissue debris, dead cells, and any pathogens. PMNs also release cytokines/ chemokines that control the intensity of the acute inflammation and recruit monocytes from circulation that differentiate to MOs in the tissue. Acute inflammation normally resolves within 1-4 days.
Atmospheric fine particulate matter and epithelial mesenchymal transition in pulmonary cells: state of the art and critical review of the in vitro studies
Published in Journal of Toxicology and Environmental Health, Part B, 2020
Margaux Cochard, Frédéric Ledoux, Yann Landkocz
Inflammation is one of the other well-known mechanisms involved in PM-mediated toxicity. The inflammatory response is a multistep physiological function. First, resident cells recognize pathogens or an injury through pattern recognition receptors (PRR) that include membrane (Toll-like receptors, TLR) or cytosolic receptors (NOD-like receptors, NLR). Binding to those receptors activates signaling pathways, inducing translocation to the nucleus of transcription factors such as NF-κB. Subsequently, transcription factors promote expression of pro-inflammatory mediators: cytokines (interleukins (IL)-6, IL-1β and tumor necrosis factor α (TNFα)), chemokines (IL-8, CCL2), enzymes (COX2) and adhesion molecules (VCAM, ICAM-1). Finally, pro-inflammatory mediators secreted by cells induce an inflammatory response via recruitment of immune cells (Arooj et al. 2020). After exposure of A549, adenocarcinoma alveolar cells, and BEAS-2B, bronchial immortalized cells, to PM2.5in vitro, rise in IL-6, IL-1β, TNFα and IL-8 expression occurred (Dieme et al. 2012; Michael, Montag, and Dott 2013; Thomson et al. 2015).
Development of an immunosuppressive camouflage-coating platform with nanocellulose and cell membrane vesicles
Published in Journal of Biomaterials Science, Polymer Edition, 2020
Akihiro Nishiguchi, Tetsushi Taguchi
One of the most important aspects for the design of advanced biomaterials is achieving the suppression of host inflammatory responses to implanted biomaterials [1, 2]. Biomaterials that aim to compensate mechanical and biological functionality in the body are usually recognized as foreign materials once they are in contact with cells/tissues or are implanted in the body. An initial response is mounted by initiating sensing of the foreign bodies by pattern recognition receptors (PRRs) that recognize the pathogen-associated molecular patterns (PAMPs) and/or damage-associated molecular patterns (DAMPs) [3]. These responses trigger macrophages to produce inflammatory cytokines and remove these materials by degradation or phagocytosis, which may lead to acute and chronic inflammation. For example, the perfusion of blood on polyvinyl chloride blood conduits activates neutrophils [4]. Also, polymeric insulation in a pacemaker causes cracking through monocyte-producing reactive oxygen species [5], which is typically correlated with poor clinical outcomes [6]. To suppress undesirable immune responses against biomaterials, hydrophilic coating of biomaterial surfaces has been developed. Hydrophilic coating offers anti-fouling properties to biomaterial surfaces and suppresses cell adhesion [7]. Various bioinert coating technologies using hydrophilic polymers such as poly(ethylene glycol) [8], poly(2-methacryloyl oxyethyl phosphorylcholine) [9, 10], poly(2-hydroxyethyl methacrylate) [11], and betaine polymer [12] have been studied to achieve biocompatible interfaces with an ability to suppress inflammatory responses and improve long-term stability and integrity of biomedical devices implanted within tissues. To further develop the coating technology for an implant, advanced designs for biologically active surfaces such as drug-eluting coats and immunosuppressive polymers that can be sensed by immune cells and thus elicit anti-inflammatory responses are required [13, 14].