ArticleJournal of immunology (Baltimore, Md. : 1950)2016
Siglec-E Negatively Regulates the Activation of TLR4 by Controlling Its Endocytosis.
Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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Who cites it
15 citing papers in PubMed, 33 citations in OpenAlex.
- Interplay between CD33 and TREM2 in Alzheimer's Disease: Potential Mechanistic Insights into Microglial Function in Amyloid Pathology.ACS chemical neuroscience · 2026Review
- Siglec-7 inhibits TLR3-induced pro-inflammatory cytokine production from human monocytes and macrophages.Frontiers in immunology · 2026Article
- Article
- Sialic acid in the regulation of blood cell production, differentiation and turnover.Immunology · 2024Review
- RNA Sequencing of Whole Blood in Premature Coronary Artery Disease: Identification of Novel Biomarkers and Involvement of T Cell Imbalance.Journal of cardiovascular translational research · 2024Article
- Simultaneous control of infection and inflammation with keratin-derived antibacterial peptides targeting TLRs and co-receptors.Science translational medicine · 2023Article
- Ablation of Siglec-E augments brain inflammation and ischemic injury.Journal of neuroinflammation · 2022Article
- Sialylation of TLR2 initiates osteoclast fusion.Bone research · 2022Article
- The role of the Siglec-G ITIM domain during bacterial infection.Cellular and molecular biology (Noisy-le-Grand, France) · 2022Article
- Prevention of vascular-allograft rejection by protecting the endothelial glycocalyx with immunosuppressive polymers.Nature biomedical engineering · 2021Article
- Polysialic acid and Siglec-E orchestrate negative feedback regulation of microglia activation.Cellular and molecular life sciences : CMLS · 2021Article
- Interplay Between Sialic Acids, Siglec-E, and Neu1 Regulates MyD88- and TRIF-Dependent Pathways for TLR4-Activation DuringFrontiers in immunology · 2021Article
- Overexpression of Toll-like Receptor 4-linked Mitogen-activated Protein Kinase Signaling Contributes to Internalization ofInternational journal of biological sciences · 2018Article
- Expression of Siglec-E Alters the Proteome of Lipopolysaccharide (LPS)-Activated Macrophages but Does Not Affect LPS-Driven Cytokine Production or Toll-Like Receptor 4 Endocytosis.Frontiers in immunology · 2017Article
- Sialic Acids in the Immune Response during Sepsis.Frontiers in immunology · 2017Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
TLR4 signaling is critical for providing effective immune protection, but it must be tightly controlled to avoid inflammation-induced pathology. Previously, we reported extensive and direct interactions between TLR and Siglec families of pattern recognition receptors. In this study, we examined the biological significance of this interaction during infection. We show that Siglec-E is required for Escherichia coli-induced endocytosis of TLR4. Siglec-E-deficient dendritic cells infected with E. coli fail to internalize TLR4. This leads to sustained TLR4 on the cell surface and activation of NF-κB and MAPK p38, resulting in high levels of TNF-α and IL-6 compared with wild-type dendritic cells. In contrast to the signaling events occurring at the plasma membrane, as a result of the inability to internalize TLR4, Siglec-E-deficient dendritic cells were also defective for TRIF-mediated IFN-β production in response to E. coli infection. Furthermore, we found that accumulation of ubiquitinated TLR4 and binding of E3 ubiquitin ligase Triad3A to TLR4 was increased significantly in bone marrow-derived dendritic cells from wild-type mice, but not from Siglec-E-deficient mice, after E. coli infection. This represents a newly discovered mechanism that regulates the signaling of TLR4 during E. coli infection.
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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.