ArticleJournal of leukocyte biology2009
Pivotal Advance: Toll-like receptor regulation of scavenger receptor-A-mediated phagocytosis.
Article in Journal of leukocyte biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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
49 citing papers in PubMed, 87 citations in OpenAlex.
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- Flagellate bacteria-mediated tumour antigen delivery: A novel approach to enhance dendritic cell activation for in situ cancer vaccination.Microbial biotechnology · 2024Review
- Pathways for macrophage uptake of cell-free circular RNAs.Molecular cell · 2024Article
- Specific interaction between Group BInfection and immunity · 2024Article
- Porous Precision-Templated 40 μm Pore Scaffolds Promote Healing through Synergy in Macrophage Receptor with Collagenous Structure and Toll-Like Receptor Signaling.Tissue engineering. Part A · 2024Article
- Toll-like receptor 4 and macrophage scavenger receptor 1 crosstalk regulates phagocytosis of a fungal pathogen.Nature communications · 2023Article
- Recognition of Arboviruses by the Mosquito Immune System.Biomolecules · 2023Review
- Article
- Scavenger receptors in host defense: from functional aspects to mode of action.Cell communication and signaling : CCS · 2022Review
- Role of macrophage scavenger receptor MSR1 in the progression of non-alcoholic steatohepatitis.Frontiers in immunology · 2022Review
- TLR2 Potentiates SR-Marco-Mediated Neuroinflammation by Interacting with the SRCR Domain.Molecular neurobiology · 2021Article
- Differential Enhancement of Neutrophil Phagocytosis by Anti-Bactericidal/Permeability-Increasing Protein Antibodies.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- Identification of cell-surface glycans that mediate motility-dependent binding and internalization of Pseudomonas aeruginosa by phagocytes.Molecular immunology · 2021Article
- Bactericidal/Permeability-Increasing Protein Preeminently Mediates Clearance ofFrontiers in immunology · 2021Article
- Phagocytosis-Inflammation Crosstalk in Sepsis: New Avenues for Therapeutic Intervention.Shock (Augusta, Ga.) · 2020Review
- Macrophage scavenger receptor 1 controls Chikungunya virus infection through autophagy in mice.Communications biology · 2020Article
- Resistin-Inhibited Neural Stem Cell-Derived Astrocyte Differentiation Contributes to Permeability Destruction of the Blood-Brain Barrier.Neurochemical research · 2019Article
- Phosphatidylinositol-(3,4,5)-Trisphosphate Induces Phagocytosis of Nonmotile Pseudomonas aeruginosa.Infection and immunity · 2018Article
- More Than Just a Removal Service: Scavenger Receptors in Leukocyte Trafficking.Frontiers in immunology · 2018Review
- CCancer nanotechnology · 2018Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Class-A scavenger receptors (SR-A) and TLR mediate early immune responses against pathogenic bacteria. SR-A and TLR molecules are expressed on phagocytes and interact with common ligands from Gram-negative and Gram-positive bacteria; however, the contribution of TLR activity to SR-A-mediated phagocytosis has not been assessed directly. Herein, we provide genetic and functional evidence that ligand- and TLR-specific stimuli synergize with SR-A to mediate bacterial phagocytosis. Although complete loss of SR-A (SR-A(-/-)) is known to impair bacterial clearance, here we identify the first deficiency attributable to SR-A heterozygosity: SR-A(+/-)TLR4(+/-) cells and mice are impaired significantly in the clearance of Gram-negative Escherichia coli. This phenotype is specific to the TLR signaling event, as SR-A(+/-)TLR4(+/-) cells are not deficient for the clearance of Gram-positive Staphylococcus aureus bacteria, which contain cell-surface TLR2 ligands but lack TLR4 ligands. We demonstrate that this is a global, phagocytic mechanism, regulated independently by multiple TLRs, as analogous to the SR-A(+/-)TLR4(+/-) deficit, SR-A(+/-)TLR2(+/-) cells are impaired for S. aureus uptake. In support of this, we show that SR-A(+/-)MyD88(+/-) cells recapitulate the phagocytosis defect observed in SR-A(+/-)TLR4(+/-) cells. These data identify for the first time that TLR-driven innate immune responses, via a MyD88 signaling mechanism, regulate SR-A-dependent phagocytosis of bacteria. These findings provide novel insights into how innate immune cells control SR-A-mediated trafficking and are the first demonstration that subtle changes in the expression of SR-A and TLRs can substantially affect host bacterial clearance.
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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.