ArticleThe Journal of biological chemistry2020
An alternative model for type I interferon induction downstream of human TLR2.
Article in The Journal of biological chemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- Overweight and obesity induce Toll-like receptor 2-induced Type I IFN signaling.npj metabolic health and disease · 2026Article
- Nano-Enabled Systemic Delivery of STING Agonist by Engineered Silicasome for Potent Antitumor Immunotherapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Extracellular vesicles derived from Enterococcus faecalis: inflammatory activation does not require internalization.Cell communication and signaling : CCS · 2026Article
- TGFβ primes alveolar-like macrophages to induce type I IFN following TLR2 activation.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Endosome restricted human TLR1 polymorphism highlights a role for MyD88 in Pam3CSK4 detection.PloS one · 2026Article
- Pattern Recognition Receptors (PRRs) Expression and Activation in COVID-19 and Long COVID: From SARS-CoV-2 Escape Mechanisms to Emerging PRR-Targeted Immunotherapies.Microorganisms · 2025Review
- Type I interferons in bacterial diseases: myeloid cells at the crossroads of protection and pathology.Frontiers in immunology · 2025Review
- Label-free biosensor assay decodes the dynamics of Toll-like receptor signaling.Nature communications · 2024Article
- Review
- Truncating NFKB1 variants cause combined NLRP3 inflammasome activation and type I interferon signaling and predispose to necrotizing fasciitis.Cell reports. Medicine · 2024Article
- Borrelia burgdorferi Engages Mammalian Type I IFN Responses via the cGAS-STING Pathway.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Article
- Article
- Pim1 promotes IFN-β production by interacting with IRF3.Experimental & molecular medicine · 2022Article
- An Attenuated Strain of Human Cytomegalovirus for the Establishment of a Subviral Particle Vaccine.Vaccines · 2022Article
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- Anti-Inflammatory Effect of anInternational journal of molecular sciences · 2022Article
- Single-cell analysis of myeloid cells in HPVFrontiers in immunology · 2022Article
- Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Surface-exposed Toll-like receptors (TLRs) such as TLR2 and TLR4 survey the extracellular environment for pathogens. TLR activation initiates the production of various cytokines and chemokines, including type I interferons (IFN-I). Downstream of TLR4, IFNβ secretion is only vigorously triggered in macrophages when the receptor undergoes endocytosis and switches signaling adaptor; surface TLR4 engagement predominantly induces proinflammatory cytokines via the signaling adaptor MyD88. It is unclear whether this dichotomy is generally applicable to other TLRs, cell types, or differentiation states. Here, we report that diverse TLR2 ligands induce an IFN-I response in human monocyte-like cells, but not in differentiated macrophages. This TLR2-dependent IFN-I signaling originates from the cell surface and depends on MyD88; it involves combined activation of the transcription factors IRF3 and NF-κB, driven by the kinases TBK1 and TAK1-IKKβ, respectively. TLR2-stimulated monocytes produced modest IFNβ levels that caused productive downstream signaling, reflected by STAT1 phosphorylation and expression of numerous interferon-stimulated genes. Our findings reveal that the outcome of TLR2 signaling includes an IFN-I response in human monocytes, which is lost upon macrophage differentiation, and differs mechanistically from IFN-I-induction through TLR4. These findings point to molecular mechanisms tailored to the differentiation state of a cell and the nature of receptors activated to control and limit TLR-triggered IFN-I responses.
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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.