ArticleThe Biochemical journal2004
Combinational clustering of receptors following stimulation by bacterial products determines lipopolysaccharide responses.
Article in The Biochemical journal, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
45 citing papers in PubMed, 137 citations in OpenAlex.
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- Matrix lumican endocytosed by immune cells controls receptor ligand trafficking to promote TLR4 and restrict TLR9 in sepsis.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Homeostatic and pathogenic roles of GM3 ganglioside molecular species in TLR4 signaling in obesity.The EMBO journal · 2020Article
- Lipid-Protein and Protein-Protein Interactions in the Pulmonary Surfactant System and Their Role in Lung Homeostasis.International journal of molecular sciences · 2020Review
- Criticality of plasma membrane lipids reflects activation state of macrophage cells.Journal of the Royal Society, Interface · 2020Article
- Article
- Monophosphoryl lipid A induces protection against LPS in medullary thick ascending limb through a TLR4-TRIF-PI3K signaling pathway.American journal of physiology. Renal physiology · 2017Article
- Soluble CD83 Inhibits T Cell Activation by Binding to the TLR4/MD-2 Complex on CD14Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Co-operation of TLR4 and raft proteins in LPS-induced pro-inflammatory signaling.Cellular and molecular life sciences : CMLS · 2015Review
- BK channels regulate myometrial contraction by modulating nuclear translocation of NF-κB.Endocrinology · 2014Article
- Pseudomonas aeruginosa flagellar motility activates the phagocyte PI3K/Akt pathway to induce phagocytic engulfment.American journal of physiology. Lung cellular and molecular physiology · 2014Article
- An alanine-to-proline mutation in the BB-loop of TLR3 Toll/IL-1R domain switches signalling adaptor specificity from TRIF to MyD88.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- CD14 mediates binding of high doses of LPS but is dispensable for TNF-α production.Mediators of inflammation · 2013Article
- Statins decrease lung inflammation in mice by upregulating tetraspanin CD9 in macrophages.PloS one · 2013Article
- Characterization of differential Toll-like receptor responses below the optical diffraction limit.Small (Weinheim an der Bergstrasse, Germany) · 2012Article
- Toll-like receptor 2 is required for LPS-induced Toll-like receptor 4 signaling and inhibition of ion transport in renal thick ascending limb.The Journal of biological chemistry · 2012Article
- Toll-like receptor activation of human cells by synthetic triacylated lipid A-like molecules.The Journal of biological chemistry · 2012Article
- Titanium particles activate toll-like receptor 4 independently of lipid rafts in RAW264.7 murine macrophages.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2011Article
- Location, location, location: is membrane partitioning everything when it comes to innate immune activation?Mediators of inflammation · 2011Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
The innate immune system has the capacity to recognize a wide range of pathogens based on conserved PAMPs (pathogen-associated molecular patterns). In the case of bacterial LPS (lipopolysaccharide) recognition, the best studied PAMP, it has been shown that the innate immune system employs at least three cell-surface receptors: CD14, TLR4 (Toll-like receptor 4) and MD-2 protein. CD14 binds LPS from Enterobacteriaceae and then transfers it to MD-2, leading to TLR4 aggregation and signal transduction. LPS analogues such as lipid IVa seem to act as LPS antagonists in human cells, but exhibit LPS mimetic activity in mouse cells. Although TLR4 has been shown to be involved in this species-specific discrimination, the mechanism by which this is achieved has not been elucidated. The questions that remain are how the innate immune system can discriminate between LPS from different bacteria as well as different LPS analogues, and whether or not the structure of LPS affects its interaction with the CD14-TLR4-MD-2 cluster. Is it possible that the 'shape' of LPS induces the formation of different receptor clusters, and thus a different immune response? In the present study, we demonstrate using biochemical as well as fluorescence-imaging techniques that different LPS analogues trigger the recruitment of different receptors within microdomains. The composition of each receptor cluster as well as the number of TLR4 molecules that are recruited within the cluster seem to determine whether an immune response will be induced or inhibited.
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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.