NOD1 and NOD2: signaling, host defense, and inflammatory disease.
By R. Caruso, N. Warner, N. Inohara, G. Núñez. Immunity, 2014
750 citations recorded by the source corpus.
The nucleotide-binding oligomerization domain (NOD) proteins NOD1 and NOD2, the founding members of the intracellular NOD-like receptor family, sense conserved motifs in bacterial peptidoglycan and induce proinflammatory and antimicrobial responses. Here, we discuss recent developments about the mechanisms by which NOD1 and NOD2 are activated by bacterial ligands, the regulation of their signaling pathways, and their role in host defense and inflammatory disease. Several routes for the entry of peptidoglycan ligands to the host cytosol to trigger activation of NOD1 and NOD2 have been elucidated. Furthermore, genetic screens and biochemical analyses have revealed mechanisms that regulate NOD1 and NOD2 signaling. Finally, recent studies have suggested several mechanisms to account for the link between NOD2 variants and susceptibility to Crohn's disease. Further understanding of NOD1 and NOD2 should provide new insight into the pathogenesis of disease and the development of new strategies to treat inflammatory and infectious disorders.
Subfields: Immunology
View Paper: https://www.semanticscholar.org/paper/de359e209d6ae0753b107826ab3a19bca8f4cdd9
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In Immunology
Citations in the corpus
- Pattern recognition receptors in health and diseases (2021, background): “The known mechanism is that NOD2 activates NF-κB, JAK2/STAT3, and MAPK pathways in a RIP2dependent manner, leading to liver inflammation.(351) It is worth noting that activated NOD2 can also act as the initiator of the nuclear autophagy pathway that does not depend on RIP2, thereby promoting the deg”
- Gut microbiota: Role in pathogen colonization, immune responses, and inflammatory disease (2017, background): “responses in Paneth cells or an altered intraepithelial autophagy (216).”
- Phagocytosis: An Immunobiologic Process. (2016, background): “Crohn’s disease, for example, has a genetic component involving Nod-like receptors and autophagy (Caruso et al., 2014).”