ArticlePLoS pathogens2009
Cross-talk between TLR4 and FcgammaReceptorIII (CD16) pathways.
Article in PLoS pathogens, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 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.
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Who cites it
54 citing papers in PubMed, 85 citations in OpenAlex.
- Human resistin promotes neutrophil proinflammatory activation and neutrophil extracellular trap formation and increases severity of acute lung injury.Journal of immunology (Baltimore, Md. : 1950) · 2014Trial
- Nanocluster-mediated signaling crosstalk between FcγR and TLR4 in macrophage inflammatory responses.Scientific reports · 2025Article
- Acetylation of TIR domains in the TLR4-Mal-MyD88 complex regulates immune responses in sepsis.The EMBO journal · 2024Article
- Direct Binding of Bovine IgG-Containing Immune Complexes to Human Monocytes and Their Putative Role in Innate Immune Training.Nutrients · 2022Article
- Immobile ligands enhance FcγR-TLR2/1 crosstalk by promoting interface overlap of receptor clusters.Biophysical journal · 2022Article
- Detection and functional resolution of soluble immune complexes by an FcγR reporter cell panel.EMBO molecular medicine · 2022Article
- Toll-Like Receptor 4: A Promising Therapeutic Target for Alzheimer's Disease.Mediators of inflammation · 2022Review
- The Functional Role of IgA in the IgM/IgA-Enriched Immunoglobulin Preparation Trimodulin.Biomedicines · 2021Article
- Cholesterol and sphingomyelin are critical for Fcγ receptor-mediated phagocytosis of Cryptococcus neoformans by macrophages.The Journal of biological chemistry · 2021Article
- Spatial organization of FcγR and TLR2/1 on phagosome membranes differentially regulates their synergistic and inhibitory receptor crosstalk.Scientific reports · 2021Article
- Lipopolysaccharide-Enhanced Responses against Aryl Hydrocarbon Receptor in FcgRIIb-Deficient Macrophages, a Profound Impact of an Environmental Toxin on a Lupus-Like Mouse Model.International journal of molecular sciences · 2021Article
- Prominent Indomethacin-Induced Enteropathy in FcgriibInternational journal of molecular sciences · 2021Article
- Acute Kidney Injury Induced Lupus Exacerbation Through the Enhanced Neutrophil Extracellular Traps (and Apoptosis) in Fcgr2b Deficient Lupus Mice With Renal Ischemia Reperfusion Injury.Frontiers in immunology · 2021Article
- Tumor necrosis factor α inhibition overcomes immunosuppressive M2b macrophage-induced bevacizumab resistance in triple-negative breast cancer.Cell death & disease · 2020Article
- Prolyl Oligopeptidase FromFrontiers in microbiology · 2020Article
- Polymorphisms in Fc Gamma Receptors and Susceptibility to Malaria in an Endemic Population.Frontiers in immunology · 2020Review
- Geometrical reorganization of Dectin-1 and TLR2 on single phagosomes alters their synergistic immune signaling.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- FcRγ deficiency improves survival in experimental sepsis by down-regulating TLR4 signaling pathway.Immunologic research · 2019Article
- Inside-Out Control of Fc-Receptors.Frontiers in immunology · 2019Review
- Impact of CD14 on Reactive Oxygen Species Production from Human Leukocytes Primed byOxidative medicine and cellular longevity · 2019Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
Abstract
Pathogen-pattern-recognition by Toll-like receptors (TLRs) and pathogen clearance after immune complex formation via engagement with Fc receptors (FcRs) represent central mechanisms that trigger the immune and inflammatory responses. In the present study, a linkage between TLR4 and FcgammaR was evaluated in vitro and in vivo. Most strikingly, in vitro activation of phagocytes by IgG immune complexes (IgGIC) resulted in an association of TLR4 with FcgammaRIII (CD16) based on co-immunoprecipitation analyses. Neutrophils and macrophages from TLR4 mutant (mut) mice were unresponsive to either lipopolysaccharide (LPS) or IgGIC in vitro, as determined by cytokine production. This phenomenon was accompanied by the inability to phosphorylate tyrosine residues within immunoreceptor tyrosine-based activation motifs (ITAMs) of the FcRgamma-subunit. To transfer these findings in vivo, two different models of acute lung injury (ALI) induced by intratracheal administration of either LPS or IgGIC were employed. As expected, LPS-induced ALI was abolished in TLR4 mut and TLR4(-/-) mice. Unexpectedly, TLR4 mut and TLR4(-/-) mice were also resistant to development of ALI following IgGIC deposition in the lungs. In conclusion, our findings suggest that TLR4 and FcgammaRIII pathways are structurally and functionally connected at the receptor level and that TLR4 is indispensable for FcgammaRIII signaling via FcRgamma-subunit activation.
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What OpenQuestion holds
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.