Toll-like Receptor Ligand
Toll-like Receptor Ligand - Related Videos
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.
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.
05:57
Biomembrane Force Probe to Quantitate Receptor-Ligand Interactions
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2025
In this video, biomembrane force probes (BFPs) are used to measure the forces between receptors and ligands. This technique can detect interactions by monitoring the pressure needed to break the bonds between the pMHC conjugated on the probe beads and the TCRs on the target cells.
FAQs
Recognition initiates a coordinated signaling sequence rather than an immediate immune output. The receptor dimerizes and recruits adaptor proteins, including MyD88 or TRIF. These adaptors connect ligand recognition to transcription factors such as NF-κB and interferon-regulatory factors, which then drive production of inflammatory cytokines and type I interferons. This sequence converts molecular detection into an early defense response.
The overview identifies both the cell surface and endosomes as sites of ligand recognition, indicating that cellular location is an important part of innate immune detection. A ligand encountered in either compartment can promote receptor dimerization and downstream signaling, but the resulting response is organized through adaptor recruitment and transcription-factor activation. This compartment-based arrangement helps cells detect microbial patterns in different cellular contexts.
MyD88 and TRIF function as adaptor proteins that connect activated receptors to intracellular signaling. After receptor dimerization, recruitment of one or both adaptors helps transmit the recognition signal toward NF-κB and interferon-regulatory factors. Their involvement explains how ligand binding can produce coordinated inflammatory cytokine and type I interferon responses rather than remaining a receptor-level event.
The downstream transcription factors activated after ligand recognition help shape the response. NF-κB is associated in the overview with induction of inflammatory cytokines, while interferon-regulatory factors are linked with type I interferon production. Because receptor recognition can recruit signaling adaptors that activate these transcription factors, the response can coordinate inflammatory and antiviral signaling outputs during early innate defense.
Researchers can use the defined immune-stimulating activity of these ligands to investigate how cells detect conserved pathogen-associated patterns and initiate early defense responses. Experiments can focus on the connection between receptor recognition, adaptor recruitment, transcription-factor activation, and induction of cytokines or type I interferons. This makes the ligands useful tools for studying innate immune signaling in a controlled biological context.
Synthetic ligands are valuable because their immune-stimulating activity can be examined as a defined experimental input. In vaccine adjuvant development, that activity provides a way to investigate how receptor-triggered innate signaling might support immune activation alongside vaccination. The same principle also supports infection research and studies of inflammatory or autoimmune disease mechanisms, where altered early defense signaling is relevant.