Toll‐like receptors control autophagy

By Mônica A Delgado, Rasha A Elmaoued, Alexander S. Davis, George B. Kyei, V. Deretic. EMBO Journal, 2008

754 citations recorded by the source corpus.

Subfields: Endocrinology, Epidemiology, Pharmacology

View Paper: https://www.semanticscholar.org/paper/5f0d1587eb7b46d67423fa2c643e311cf5a58353

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Endocrinology

1. Beth Levine
2. D. Klionsky
3. Congcong He
4. G. Núñez
5. V. Deretic
6. N. Mizushima

In Epidemiology

1. Beth Levine
2. D. Klionsky
3. V. Deretic
4. D. Tang
5. R. Kang
6. Guido Kroemer
7. I. Slaninová
8. N. Mizushima

In Pharmacology

1. D. Klionsky
2. Beth Levine
3. V. Deretic
4. Congcong He
5. D. Tang
6. R. Kang
7. G. Núñez
8. N. Mizushima

Citations in the corpus

• Autophagy in inflammation, infection, and immunometabolism (2021, background): “Of note, TLR3 and dsRNA ligands induce autophagy (Delgado et al., 2008), whereas TBK1 plays a role in autophagy (Kumar et al.”
• 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].”
• PAMPs and DAMPs: Signal 0s that Spur Autophagy and Immunity (2012, background): “The Toll/interleukin-1 receptor homologous region (TIR) adapter proteins [myeloid differentiation factor 88 (MyD88), TIR adapter protein (TIRAP)/MyD88 adapter-like (MAL), translocating chain-associated membrane protein (TRAM), and TIR-domain-containing adapter-inducing interferon-b (TRIF)] also appe”
• Antimicrobial mechanisms of phagocytes and bacterial evasion strategies (2009, background): “This autophagic response can be enhanced by Toll-like receptor ligand”
• Activation of Autophagy by Inflammatory Signals Limits IL-1β Production by Targeting Ubiquitinated Inflammasomes for Destruction (2012, positive): “In macrophages, autophagy can be triggered by the engagement of Toll-like receptor”
• Autophagy: a lysosomal degradation pathway with a central role in health and disease. (2009, background): “Thus, engaging the autophagy pathway via TLR signaling (especially TLR7 through its binding to single-stranded RNA) enhances phagosome maturation and destruction of pathogens [157].”
• Dying for a cause: NETosis, mechanisms behind an antimicrobial cell death modality (2011, positive): “receptors, including Toll-like receptors (TLR) and nucleotidebinding and oligomerization domain (NOD)-like receptors (NLR), induce autophagy in macrophages.(74,75) Mitroulis et al.”
• Exploring autophagy with Gene Ontology (2016, background): “Toll-Like Receptor (TLR) signaling in general links autophagy to innate immunity [34], with TLR4 signaling shown to induce autophagy via BECN1 [38].”
• NOD2 stimulation induces autophagy in dendritic cells influencing bacterial handling and antigen presentation (2010, background): “Recently, it has been shown that signaling through TLRs can lead to autophagosome formatio”
• Autophagy, Immunity, and Microbial Adaptations (2009, background): “Autophagy is proinflammatory, e.g., when autophagy captures cytosolic viral replication intermediates and delivers them to the lumen of endosomal compartments where they meet their cognate PRRs, as in the case with viral single-stranded RNA and Toll-like receptor (TLR) 7 (Lee et al., 2007).”