NOD2 stimulation induces autophagy in dendritic cells influencing bacterial handling and antigen presentation

By R. Cooney, J. Baker, O. Brain, B. Danis, T. Pichulik, P. Allan, D. Ferguson, B. Campbell, D. Jewell, A. Simmons. Nature Medicine, 2010

1,089 citations recorded by the source corpus.

Subfields: Epidemiology, Immunology

View Paper: https://www.semanticscholar.org/paper/8e09ea422bf06f465ec5edbc9c7f3d68cfbfe9ab

How researchers see this paper

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In Epidemiology

1. D. Tang
2. R. Kang
3. F. Powrie
4. H. J. Zeh
5. Michael Lotze
6. Carolyn B. Coyne
7. Haitao Wen
8. Ramnik J. Xavier

In Immunology

1. F. Powrie
2. H. J. Zeh
3. D. Tang
4. R. Kang
5. K. Papadakis
6. Michael Lotze
7. K. Maloy
8. G. Ramos

Citations in the corpus

• Intestinal homeostasis and its breakdown in inflammatory bowel disease (2011, background): “Recent studies have found that NOD2 stimulates autophagy by interacting directly with ATG16L1, which allows the recruitment of ATG16L1 to sites of bacterial entr”
• Genetics and pathogenesis of inflammatory bowel disease (2011, background): “For example, MDP stimulation induces autophagy, which controls bacterial replication and antigen presentation, and acts on dendritic cells in conjunction with TLR ligands to promote T H 17-cell differentiatio”
• The gut microbiota and inflammatory bowel disease (2014, neutral): “NOD2 stimulation with MDP induces autophagy [40], which regulates replication of intracellular bacteria and is also involved in bacterial antigen presentation in the infected cells.”
• The Inflammasome NLRs in Immunity, Inflammation, and Associated Diseases (2011, background): “The biological significance of inflammasome inhibition of autophagy might be a generalized mechanism, given that other NLRs affect autophagy (79, 80).”
• Molecular definitions of autophagy and related processes (2017, neutral): “…the pattern recognition receptors nucleotide-binding oligomerization domain containing 1 (NOD1) and NOD2, which physically interact with ATG16L1 and immunity-related GTPase M (IRGM) upon recognition of bacterial muramyl dipeptide (Cooney et al , 2010; Travassos et al , 2010; Chauhan et al , 2015).”
• Vaccine adjuvants: mechanisms and platforms (2023, background): “In addition, activation of these NLRs will lead to the production of pro-inflammatory cytokines such as IL1β and IL-18, driving naive T cells to bias polarization into Th2 type cells.(48) Muramyl dipeptide (MDP) or complete Freund’s adjuvant (CFA) can activate NOD1 and NOD2 and subsequently stimulat”
• Mechanisms of Disease: Inflammatory Bowel Diseases. (2019, background): “In dendritic cells, defects in these genes also result in an impaired ability to present exogenous antigens to T-cells (26).”
• Innate and adaptive immunity in inflammatory bowel disease. (2014, background): “Interestingly, while immune stimulation via TLRs had been shown to activate autophagy [33], recent studies have linked NOD2 with autophagy induction and have shown that both NOD2 and ATG16L1 variants induce altered autophagy, antigen presentation and intracellular bacterial handling by DCs [34,35].”
• New IBD genetics: common pathways with other diseases (2011, background): “Most recently, key functional links have been elicited between NOD2 and autophagy.(38) 39 NOD2 initiates autophagy by recruiting ATG16L1 to the cell membrane at the site of bacterial entry, a process that requires RIPK2, ATG5 and ATG7.”