ArticleJournal of immunology (Baltimore, Md. : 1950)2018
Constitutively Bound EGFR-Mediated Tyrosine Phosphorylation of TLR9 Is Required for Its Ability To Signal.
Article in Journal of immunology (Baltimore, Md. : 1950), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 21 citations in OpenAlex.
- Article
- Toll-like receptor 9 arginine methylation promotes ferroptosis in prostate cancer through the NRF2/GPX4 signaling pathway.Translational andrology and urology · 2026Article
- A Novel Tyrosine Kinase Axis in Innate Immune Signaling.Viruses · 2025Review
- Article
- Targeting AnxA2-EGFR signaling: hydroxychloroquine as a therapeutic strategy for bleomycin-induced pulmonary fibrosis.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- EGFR-MEK1/2 cascade negatively regulates bactericidal function of bone marrow macrophages in mice with Staphylococcus aureus osteomyelitis.PLoS pathogens · 2024Article
- EGF-Receptor-Dependent TLR7 Signaling in Macrophages Promotes Glomerular Injury in Crescentic Glomerulonephritis.Laboratory investigation; a journal of technical methods and pathology · 2023Article
- Unexpected Need of the Epidermal Growth Factor Receptor Tyrosine Kinase Activity for Signaling by Intracellular Pattern Recognition Receptors of Nucleic Acids.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2023Review
- Development and function of chicken XCR1Frontiers in immunology · 2023Article
- Antiviral response within different cell types of the CNS.Frontiers in immunology · 2022Review
- Survival of HT29 Cancer Cells Is Affected by IGF1R InhibitionPathology oncology research : POR · 2022Article
- Human RNase3 immune modulation by catalytic-dependent and independent modes in a macrophage-cell line infection model.Cellular and molecular life sciences : CMLS · 2021Article
- EGFR-mediated tyrosine phosphorylation of STING determines its trafficking route and cellular innate immunity functions.The EMBO journal · 2020Article
- Epigenetic programming underpins B cell dysfunction in human SLE.Nature immunology · 2019Article
- Quantification of Infectious Sendai Virus Using Plaque Assay.Bio-protocol · 2018Article
- Ifi204/p204, a new piece in the sepsis puzzle.Annals of translational medicine · 2018Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Mammalian TLRs recognize microbial infection or cell death-associated danger signals and trigger the appropriate cellular response. These responses determine the strength and the outcome of the host-microbe interaction. TLRs are transmembrane proteins located on the plasma or the endosomal membrane. Their ectodomains recognize specific microbial or endogenous ligands, and the cytoplasmic domains interact with specific proteins to activate intracellular signaling pathways. TLR9, an endosomal TLR, is activated by endocytosed DNA. Activated TLR9 recruits the cytoplasmic adapter MyD88 and other signaling proteins to induce the synthesis of inflammatory cytokines and IFN. Uncontrolled activation of TLR9 leads to the undesired overproduction of inflammatory cytokines and consequent pathogenesis. Therefore, appropriate activation and the regulation of TLR9 signaling are critical. Tyrosine (Tyr) phosphorylation of TLR9 is essential for its activation; however, the role of specific Tyr kinases is not clear. In this article, we report that epidermal growth factor receptor (EGFR), a membrane-bound protein Tyr kinase, is essential for TLR9 signaling. Genetic ablation of EGFR or pharmacological inhibition of its kinase activity attenuates TLR9-mediated induction of genes in myeloid and nonmyeloid cell types. EGFR is constitutively bound to TLR9; upon ligand stimulation, it mediates TLR9 Tyr phosphorylation, which leads to the recruitment of MyD88, activation of the signaling kinases and transcription factors, and gene induction. In mice, TLR9-mediated liver injury and death are blocked by an EGFR inhibitor or deletion of the EGFR gene from myeloid cells, which are the major producers of inflammatory cytokines.
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