NOD2 is a negative regulator of Toll-like receptor 2–mediated T helper type 1 responses

By Tomohiro Watanabe, A. Kitani, P. Murray, W. Strober. Nature Immunology, 2004

924 citations recorded by the source corpus.

Subfields: Cancer Research, Immunology

View Paper: https://www.semanticscholar.org/paper/8fe0fefcd12906d6159a5bcb67804d8ddc0a6379

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In Cancer Research

1. Shizuo Akira
2. Luke A. O'Neill
3. K. Takeda
4. R. Sartor
5. R. Medzhitov
6. Taro Kawai
7. B. Beutler
8. S. Ghosh

In Immunology

1. Shizuo Akira
2. Luke A. O'Neill
3. K. Takeda
4. A. Sher
5. G. Trinchieri
6. F. Liew
7. E. Brint
8. R. Medzhitov

Citations in the corpus

• Negative regulation of Toll-like receptor-mediated immune responses (2005, background): “These results indicate that NOD2 is a negative regulator of TLR2 signallin”
• Mechanisms of Disease: pathogenesis of Crohn's disease and ulcerative colitis (2006, background): “Their investigations demonstrated that, in CARD15 -defective cells, Toll-like receptor 2 (TLR2) was unable to downregulate NFκB activation”
• Cooperation of Toll-like receptor signals in innate immune defence (2007, background): “Interestingly, the production of cytokines induced by TLR2 ligands, but not by other TLR ligands, was shown to be higher in mice deficient for NOD2 compared with wild-type mic”
• Alteration of Gut Microbiota in Inflammatory Bowel Disease (IBD): Cause or Consequence? IBD Treatment Targeting the Gut Microbiome (2019, background): “It is also speculated that CD-associated NOD2 variants might allow intracellular infiltration of bacteria and allow them to escape from immune cell phagocytosis, resulting in a high immune response [179].”
• Toll-like receptors in innate immunity. (2004, positive): “In the absence of NOD2 or the presence of a Crohn’s disease-like Nod2 mutation, TLR2-mediated activation of NF-j B, especially the cRel subunit, has been shown to be enhanced, which explains enhanced NF-j B activity and Th1 responses in Crohn’s disease patients (62).”
• Innate and adaptive immunity in inflammatory bowel disease. (2014, background): “Other studies suggest that the loss of function in NOD2 may result in the lack of inhibition of TLR2 stimulation, leading to activation of inflammatory pathways and excessive Th-1 responses [27].”
• Nod-like proteins in immunity, inflammation and disease (2006, background): “Along with observations demonstrating that Nod2-deficient mice have a general lack of responsiveness to muramyl dipeptid”
• Genes and Molecules of Lactobacilli Supporting Probiotic Action (2008, background): “showed that NOD2 can be a negative regulator of TLR2-dependent NF- B signaling (273).”
• Macrophage activation by endogenous danger signals (2008, background): “In macrophages deficient in NOD2, activation-induced translocation of NF-κB is more pronounced relative to wild-type cells [42].”