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Recognition of microbe-associated molecular patterns by pattern recognition receptors
Published in Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald, Principles of Mucosal Immunology, 2020
NOD2 is constitutively or inducibly expressed in monocytes, macrophages, T and B cells, dendritic cells, epithelial cells, and Paneth cells. In contrast, NOD1 is ubiquitously expressed in many tissues and cells. NOD2 protein has been detected throughout the cytoplasm of cells, but redistribution to the cell membrane is required for the induction of downstream effects after ligand recognition. NOD1 expression is regulated by interferon-γ (IFN-γ), and NOD2 expression by LPS, tumor necrosis factor-α (TNF-α), and IFN-γ. On activation, NOD1 and NOD2 induce the downstream production and release of chemokines and pro-inflammatory cytokines, such as TNF-α, IL-1β, and IL-6. NOD2 activation critically induces autophagy and mediates bacterial clearance. Both NOD1 and NOD2 interact with the inhibitor of apoptosis proteins cIAP1 and cIAP2.
DNA methyltransferase inhibitors increase NOD-like receptor activity and expression in a monocytic cell line
Published in Immunopharmacology and Immunotoxicology, 2022
Claire L. Feerick, Declan P. McKernan
NOD1 and NOD2 receptors transduce bacterial signals via similar pathways. Both recognize and bind specific components of the invading peptidoglycan (iE-DAP/TRI-DAP or MDP) via their LRR domains [10]. Active receptors subsequently recruit and bind the RIP2 adapter protein, via CARD-CARD interactions, which in turn is activated via auto-phosphorylation [11]. This initiates a cascade of ubiquitination and phosphorylation events leading to the liberation of the nuclear factor‐κB (NF‐κB) transcription factor from its inhibitor (IκBα) and activation of mitogen‐activating protein kinases (MAPKs) such as p38 and extracellular signal‐regulated kinase (ERK). These MAPKs are upstream promoters of the activator protein‐1 (AP1) transcription factor. NF‐κB and AP-1 transcription factors subsequently translocate to the nucleus to promote expression of pro‐inflammatory mediators including cytokines (e.g. TNF-α and IL-6) and chemokines (e.g. IL-8) [9,12].
Increased inflammatory responsiveness of peripheral blood mononuclear cells (PBMCs) to in vitro NOD2 ligand stimulation in patients with ankylosing spondylitis
Published in Immunopharmacology and Immunotoxicology, 2018
Negar Vanaki, Taghi Golmohammadi, Ahmadreza Jamshidi, Maryam Akhtari, Mahdi Vojdanian, Shayan Mostafaei, Shiva Poursani, Nooshin Ahmadzadeh, Mahdi Mahmoudi
The innate immune system provides the first and immediate response to foreign agents through pattern recognition receptors (PRRs). Members of the PRR family are able to recognize conserved molecular patterns in pathogens or signals released from stressed or damaged cells [10]. The nucleotide-binding oligomerization domain-containing protein (NOD)1 and NOD2 are two cytosolic members in this family that recognize specific peptidoglycan (PGN) structures in bacterial cell walls. NOD1 can sense meso-diaminopimelic acid (DAP) in Gram negative bacteria. However, NOD2 functions as the general sensor of bacteria by recognizing muramyl dipeptide (MDP). Following interaction with ligands, both the receptors recruit receptor-interacting protein kinase 2 (RIPK2) to initiate the transcription of proinflammatory cytokines [11,12].
Development of a PHBV nanoparticle as a peptide vehicle for NOD1 activation
Published in Drug Delivery, 2021
Mauricio Cabaña-Brunod, Pablo A. Herrera, Valeria Márquez-Miranda, Felipe M. Llancalahuen, Yorley Duarte, Danilo González-Nilo, Juan A. Fuentes, Cristián Vilos, Luis Velásquez, Carolina Otero
The innate immune system's action begins with the activation of NOD1 by the binding of its bacterial ligand (iE-DAP) to the LRR domain. This event initiates a process of auto-oligomerization in its central zone, then interacts with its protein-2 adapter molecule (RIP2, receptor-interacting protein 2), a serine/threonine kinase that binds to the CARD domain of the NOD1 receptor (Girardin et al., 2001; Kobayashi et al., 2002; Hasegawa et al., 2008). Recruitment of RIP2 at this site of interaction is essential, as it communicates the signaling cascade's initiation through NF-κB or via the mitogen-activated protein kinase (MAPK) (Ogura et al., 2001; Kobayashi et al., 2002).