Icam-1 Interaction
Icam-1 Interaction - Related Videos
11:45
Imaging of HIV-1 Envelope-induced Virological Synapse and Signaling on Synthetic Lipid Bilayers
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Cited by 4 •
2012
This article describes a method to visualize formation of an HIV-1 envelope-induced virological synapse on glass supported planar bilayers by total internal reflection fluorescence (TIRF) microscopy. The method can also be combined with immunofluorescence staining to detect activation and redistribution of signaling molecules that occur during HIV-1 envelope-induced virological synapse formation.
05:29
An In Vitro Technique to Study T Cell Interaction with Supported Planar Lipid Bilayers
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2025
This video demonstrates an in vitro technique to study immune synapse formation between primary human T cells and supported lipid bilayers (SLB). T cell surface proteins interact with respective ligands immobilized on SLB to form an immune synapse, followed by the movement of lytic granules towards the synapse, which is visualized using fluorescence microscopy.
07:40
Assay of Adhesion Under Shear Stress for the Study of T Lymphocyte-Adhesion Molecule Interactions
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Cited by 3 •
2016
This flow adhesion assay provides a simple, high impact model of T cell-epithelial cell interactions. A syringe pump is used to generate shear stress, and confocal microscopy captures images for quantification. The goal of these studies is to effectively quantify T cell adhesion using flow conditions.
08:38
Genome-wide Protein-protein Interaction Screening by Protein-fragment Complementation Assay (PCA) in Living Cells
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Cited by 27 •
2015
Proteins interact with each other and these interactions determine in a large part their functions. Protein interaction partners can be identified at high-throughput in vivo using a yeast fitness assay based on the dihydrofolate reductase protein-fragment complementation assay (DHFR-PCA).
07:39
An In vitro Co-infection Model to Study Plasmodium falciparum-HIV-1 Interactions in Human Primary Monocyte-derived Immune Cells
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Cited by 3 •
2012
We have developed an in vitro malaria-HIV-1 co-infection model to study the impact of Plasmodium falciparum on the HIV-1 replicative cycle in human primary monocyte-derived macrophages. This versatile system can easily be adapted to other primary cell types susceptible to HIV-1 infection.
FAQs
Cytokine stimulation increases ICAM-1 expression on endothelial cells, creating more opportunities for leukocyte integrins to engage the vessel surface. This change strengthens contact between circulating immune cells and the endothelium, particularly under flow, and supports subsequent movement across the vessel wall. The response therefore connects inflammatory signaling at the cell surface with altered immune-cell recruitment.
Flow tests whether molecular binding can maintain cell contact under conditions that resemble circulation. ICAM-1 binding to LFA-1 and Mac-1 can strengthen leukocyte adhesion despite movement of the surrounding fluid. Measuring adhesion under flow therefore provides information that static binding observations may not capture, helping researchers relate binding strength to the behavior of circulating immune cells.
LFA-1 and Mac-1 are leukocyte integrins that bind endothelial ICAM-1. Their engagement provides the molecular connection that allows immune cells to attach more firmly to cytokine-stimulated endothelial surfaces. Examining these integrin-mediated contacts helps researchers study how recognition between specific cell-surface partners contributes to adhesion and supports leukocyte migration across the vessel wall.
The interaction provides a measurable link between a molecular adhesion event and the movement of immune cells through vascular tissue. Binding strength influences whether leukocytes remain attached long enough to interact with the endothelium and migrate across it. Bioengineering studies can therefore use adhesion measurements to connect receptor-level recognition with larger-scale inflammatory recruitment behavior.
A model can combine cytokine-stimulated endothelial cells with circulating immune cells and a controlled contact environment. Researchers may implement this arrangement in a microfluidic platform, biomaterial, or engineered cell system, then examine how leukocytes attach to the endothelial surface. Such models reproduce selected features of vascular inflammation without requiring the full tissue environment.
Binding strength and immune-cell adhesion are central measurements because they show whether molecular contacts produce stable cell attachment. In a microfluidic or biomaterial-based system, these readouts can be related to endothelial stimulation and flow conditions. The resulting data help determine how changes in molecular recognition influence cell recruitment and migration-related behavior.
These models are useful for designing biomaterials, building microfluidic platforms, and developing engineered cell systems that reproduce aspects of vascular inflammation. They can support evaluation of immune-cell adhesion and controlled cell recruitment. By connecting engineered environments with inflammatory adhesion behavior, the approach can also inform studies of therapies for inflammatory disease.