Toll-like Receptor Signaling
Toll-like Receptor Signaling - Related Videos
03:53
An Assay to Screen Bioactive Nanoparticles for Toll-Like Receptor Signaling Inhibition
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2025
This video demonstrates a reporter cell-based assay for screening potential bioactive nanoparticles that inhibit Toll-like receptor (TLR) signaling. The assay involves introducing lipopolysaccharides (LPS) mixed with peptide-gold nanoparticle hybrids to reporter macrophages expressing the reporter proteins — secreted embryonic alkaline phosphatase (SEAP) and luciferase. The reduction of LPS-induced TLR signal mediated by the hybrids is determined by measuring the reporter signals.
09:51
Screening Bioactive Nanoparticles in Phagocytic Immune Cells for Inhibitors of Toll-like Receptor Signaling
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Cited by 6 •
2017
Toll-like receptor (TLR) signaling plays an important role in the pathophysiology of many human inflammatory diseases, and regulating TLR responses by bioactive nanoparticles is anticipated to be beneficial in many inflammatory conditions. THP-1 cell-based reporter cells provide a versatile and robust screening platform for identifying novel inhibitors of TLR signaling.
09:04
Detection of Neu1 Sialidase Activity in Regulating TOLL-like Receptor Activation
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Cited by 39 •
2010
The sialidase assay is a simple technical approach that will elucidate novel molecular mechanism(s) of TLR sensors of microbial infections and involvement in inflammatory diseases at the receptor level on the cell surface of live macrophages.
08:21
Isolation of Murine Peritoneal Macrophages to Carry Out Gene Expression Analysis Upon Toll-like Receptors Stimulation
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Cited by 78 •
2015
We describe here a simple protocol to isolate murine peritoneal macrophages. This procedure is followed by RNA extraction to carry out gene expression analysis upon Toll-like receptors stimulation.
07:58
Quantitative Imaging of Lineage-specific Toll-like Receptor-mediated Signaling in Monocytes and Dendritic Cells from Small Samples of Human Blood
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Cited by 12 •
2012
We describe use of ImageStream technology (www.amnis.com), which combines quantitative flow cytometry with simultaneous high-resolution digital imaging, to quantify cellular mechanisms of primary immune cells from well-defined patient cohorts. Our studies provide a blueprint for translational investigations to quantify lineage specific cellular responses in small samples from subject cohorts.
FAQs
Adaptor choice helps route receptor engagement into different downstream signaling patterns. MyD88 or TRIF activates kinase cascades that stimulate NF-κB and interferon regulatory factors. These transcriptional regulators then support production of inflammatory cytokines and type I interferons. Examining which adaptor and transcription-factor activities are engaged helps researchers distinguish the inflammatory and antiviral features of a response.
Microbial molecules and signals released by damaged cells provide different biological contexts for the same early-defense system. Microbial recognition connects Toll-like receptor signaling to pathogen detection, whereas damage recognition can connect it to inflammation even without a directly identified pathogen. This distinction is important when interpreting immune activation during infection, tissue injury, or inflammatory disease.
Regulation determines how strongly and in what context receptor-triggered signals influence host responses. Since the pathway can produce inflammatory cytokines and type I interferons, its control affects the balance between early defense and inflammation. Studying that regulation therefore helps explain why related signaling events are relevant not only to infection, but also to autoimmune and other inflammatory diseases.
The downstream products provide complementary readouts of Toll-like receptor pathway activity. Inflammatory cytokines reflect activation associated with NF-κB, while type I interferon production reflects activity involving interferon regulatory factors. Measuring or comparing these outcome classes can help researchers determine whether an experimental response is primarily inflammatory, antiviral, or a combination of both.
Researchers can use the pathway as a framework for connecting a microbial ligand with receptor engagement, adaptor activation, kinase signaling, transcription-factor stimulation, and immune outputs. Following this sequence helps organize studies of how pathogens are detected and how early host defenses begin. It also provides a basis for comparing responses to bacterial products, viral nucleic acids, and damage signals.
The pathway links recognition of conserved molecular patterns with early immune outputs, including inflammatory cytokines and type I interferons. That relationship makes its regulation relevant when researchers consider how vaccine-associated signals may influence host defense. Studying these pathways can therefore help place vaccine responses in the broader context of innate activation and subsequent immune protection.
This signaling system provides a common framework for studying infectious, autoimmune, and inflammatory disease. In infection research, it helps explain pathogen recognition and antimicrobial responses. In noninfectious settings, examining pathway regulation can clarify how signals associated with damage or dysregulated activation contribute to inflammation. The same framework thus connects protective immunity with possible disease-associated immune activity.