Nod2-Dependent Regulation of Innate and Adaptive Immunity in the Intestinal Tract
By Koichi S. Kobayashi, M. Chamaillard, Y. Ogura, O. Henegariu, N. Inohara, G. Núñez, R. Flavell. Science, 2005
1,911 citations recorded by the source corpus.
Subfields: Immunology, Infectious Diseases, Microbiology
View Paper: https://www.semanticscholar.org/paper/5f04928c833a0e7da518c656acf8bc5f50b5fe91
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In Immunology
In Infectious Diseases
In Microbiology
Citations in the corpus
- Recognition of microorganisms and activation of the immune response (2007, background): “In addition, these NOD proteins contribute to the initiation of the adaptive immune respons”
- Horror autoinflammaticus: the molecular pathophysiology of autoinflammatory disease (*). (2009, background): “Mice deficient in the murine Nod2 are susceptible to Listeria monocytogenes infection via the oral route and express reduced amounts of a subgroup of intestinal antimicrobial peptides known as cryptdins (175).”
- Toll-like receptor signalling in the intestinal epithelium: how bacterial recognition shapes intestinal function (2010, background): “and is lower in mice that lack the intracellular pattern recognition receptor NOD2 than wild-type mic”
- The Microbiome in Infectious Disease and Inflammation (2012, positive): “NOD2 is expressed in monocytes and Paneth cells and is required for the expression of antimicrobial proteins in Paneth cells (99).”
- Pathogen recognition and innate immunity. (2006, positive): “Consistently, macrophages lacking either NOD1 or NOD2 fail to produce cytokines in response to the corresponding ligands (Kobayashi et al., 2005).”
- Immune adaptations that maintain homeostasis with the intestinal microbiota (2010, background): “Likewise, nucleotide-binding oligomerization domain-containing protein 2 ( NOD2 ) controls the expression of a distinct subset of α-defensins and defensin-related cryptdins by Paneth cell”
- Mechanisms and consequences of intestinal dysbiosis (2017, background): “The NOD2 receptor, expressed in monocytes and Paneth cells [134], regulates commensal gut community by restricting the number of bacteria and the colonization by pathogens, especially in the terminal ileum [135].”