ArticleJournal of cellular and molecular medicine2014
A novel TLR2-triggered signalling crosstalk synergistically intensifies TNF-mediated IL-6 induction.
Article in Journal of cellular and molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- Gut Microbiota Metabolites Targeting the Immune Response in Sepsis: Mechanisms and Therapies.International journal of general medicine · 2025Review
- Toll-like receptor agonists as cancer vaccine adjuvants.Human vaccines & immunotherapeutics · 2024Review
- TNF-α Receptor Inhibitor Alleviates Metabolic and Inflammatory Changes in a Rat Model of Ischemic Stroke.Antioxidants (Basel, Switzerland) · 2021Article
- Article
- HRG switches TNFR1-mediated cell survival to apoptosis in Hepatocellular Carcinoma.Theranostics · 2020Article
- Suppression of LPS-induced inflammatory responses by the hydroxyl groups of dexamethasone.Oncotarget · 2017Article
- ΔPK oncolytic activity includes modulation of the tumour cell milieu.The Journal of general virology · 2016Article
- TLR2 Regulates Complement-Mediated Inflammation Induced by Blood Loss During Hemorrhage.Shock (Augusta, Ga.) · 2016Article
Corrections and comments
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Authors and funding
14 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Toll-like receptors (TLR) recognize pathogens and trigger the production of vigorous pro-inflammatory cytokines [such as tumour necrosis factor (TNF)] that induce systemic damages associated with sepsis and chronic inflammation. Cooperation between signals of TLR and TNF receptor has been demonstrated through the participation of TNF receptor 1 (TNFR) adaptors in endotoxin tolerance. Here, we identify a TLR2-mediated synergy, through a MyD88-independent crosstalk, which enhances subsequent TNF-mediated nuclear factor-kappa B activation and interleukin-6 induction. Membrane-associated adaptor MAL conduces the link between TNF receptor-associated factor 6 (TRAF6) and TNFR-associated death domain, leading to a distinctive K63-ubiquitinylated TRAF6 recruitment into TNFR complex. In summary, our results reveal a novel route of TLR signal that synergistically amplifies TNF-mediated responses, indicating an innovative target for inflammation manipulation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.