Toll-like Receptor 4
Toll-like Receptor 4 - Related Videos
03:53
An Assay to Screen Bioactive Nanoparticles for Toll-Like Receptor Signaling Inhibition
0 Views •
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.
09:04
Detection of Neu1 Sialidase Activity in Regulating TOLL-like Receptor Activation
0 Views •
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.
09:51
Screening Bioactive Nanoparticles in Phagocytic Immune Cells for Inhibitors of Toll-like Receptor Signaling
0 Views •
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.
08:21
Isolation of Murine Peritoneal Macrophages to Carry Out Gene Expression Analysis Upon Toll-like Receptors Stimulation
0 Views •
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
0 Views •
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
LPS recognition depends on cooperation among CD14, MD-2, and TLR4 rather than on TLR4 acting alone. CD14 and MD-2 participate in presenting or organizing the microbial signal so that TLR4 can respond. This coordinated assembly enables receptor dimerization, which serves as the molecular transition from signal recognition to intracellular immune signaling.
Dimerization is the key structural event that converts microbial recognition into an active receptor state. Once the TLR4 complex dimerizes after LPS engagement, it can initiate downstream signaling through both MyD88-dependent and TRIF-dependent routes. Studying this step helps explain how an extracellular bacterial signal produces coordinated changes in inflammatory and host-defense gene expression.
The two downstream branches allow TLR4 activation to influence more than one type of transcriptional response. MyD88-dependent and TRIF-dependent signaling together promote activation of NF-κB and interferon regulatory factors, linking microbial detection with inflammatory gene expression and additional host-defense programs. Comparing these branches helps researchers analyze how one receptor coordinates distinct aspects of innate immunity.
TLR4 provides a biological framework for examining how innate immune activation contributes to both infection and tissue damage. Its signaling can be studied as a sequence from recognition through pathway activation to inflammatory gene expression. This connection makes the receptor relevant when researchers investigate why immune responses that protect the host may also participate in chronic inflammation or excessive activation.
A study may follow the pathway from LPS engagement with CD14 and MD-2 through TLR4 dimerization, activation of MyD88-dependent and TRIF-dependent signaling, and induction of NF-κB or interferon regulatory factors. Examining these linked stages helps investigators determine how microbial signals are converted into measurable inflammatory gene-expression outcomes and where pathway modulation may occur.
TLR4 research supports several distinct biological applications because its signaling links microbial detection to inflammatory gene expression. In sepsis studies, investigators consider excessive immune activation; in chronic-inflammation research, they examine persistent inflammatory signaling; and in vaccine research, they assess innate immune responses. These findings can also inform strategies designed to modulate harmful activation.