Immune Cell Trafficking
Immune Cell Trafficking - Related Videos
09:22
Monitoring Immune Cells Trafficking Fluorescent Prion Rods Hours after Intraperitoneal Infection
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Cited by 6 •
2010
Here we describe a novel assay for monitoring prion uptake and trafficking by immune cells immediately following intraperitoneal inoculation by purifying and fluorescently labeling aggregated prion rods from infected brain material then monitoring their uptake and movement from the injection site and characterizing the cells mediating these events.
11:27
Analysis of SCAP N-glycosylation and Trafficking in Human Cells
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Cited by 17 •
2016
We describe a modified method for membrane fraction isolation from human cells and sample preparation for the detection of SCAP N-glycosylation and total protein by using western blot. We further introduce a GFP-labeling method to monitor SCAP trafficking using confocal microscopy. This protocol can be used in regular biology laboratories.
07:26
Isolation of Functional Cardiac Immune Cells
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Cited by 9 •
2011
This method for isolating functional immune cells from the heart provides an alternative to the conventional methods of collagenase digestion, which causes unwanted immune cell activation, resulting in a decreased responsiveness of these cells. Our method of isolation yields functional cardiac immune cells by avoiding problems associated with enzymatic digestion.
15:39
Studying Organelle Dynamics in B Cells During Immune Synapse Formation
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Cited by 8 •
2019
Herein we describe two approaches to characterize cell polarization events in B lymphocytes during the formation of an IS. The first, involves quantification of organelle recruitment and cytoskeleton rearrangements at the synaptic membrane. The second is a biochemical approach, to characterize changes in composition of the centrosome, which undergoes polarization to the immune synapse.
07:55
Imaging the Intracellular Trafficking of APP with Photoactivatable GFP
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Cited by 6 •
2015
While the transport of cell surface proteins is relatively easily studied, visualizing the trafficking of intracellular proteins is much more difficult. Here, we use constructs incorporating photoactivatable GFP and demonstrate a method to accurately follow the amyloid precursor protein from the Golgi apparatus to down-stream compartments and follow its clearance.
FAQs
Selectins create transient contacts between circulating leukocytes and the vascular endothelium, producing the rolling phase rather than immediate arrest. This slows cells sufficiently for tissue-derived signals to influence their next behavior. Without this initial, reversible interaction, leukocytes would have less opportunity to receive the chemokine signals that prepare them for stronger attachment and movement into affected tissue.
Chemokines presented during rolling activate leukocyte integrins, changing the cells’ adhesive behavior. Activated integrins then support firm attachment to the endothelium, replacing the weak, transient contacts produced by selectins. This transition is essential because it positions leukocytes for the next step, diapedesis, rather than allowing them to continue circulating past the tissue signal.
Signals originating in tissues help determine which circulating leukocytes are recruited and when recruitment occurs. Infection, injury, and cancer can each create local conditions that direct cells toward affected sites. The resulting trafficking pattern supports immune surveillance and defense, but persistent or poorly regulated signals may instead promote chronic inflammation, autoimmunity, or tissue damage.
The sequence proceeds through increasingly stable interactions: selectins initiate rolling, chemokines activate leukocyte integrins, integrins establish firm adhesion, and the attached cell then crosses the vessel wall by diapedesis. Each stage prepares the next, creating a controlled progression from bloodstream circulation to tissue localization. This order helps coordinate immune-cell access rather than producing indiscriminate infiltration.
Therapeutic strategies can either enhance protective immune recruitment or limit harmful leukocyte infiltration. Increasing recruitment may support defense where immune access is beneficial, whereas reducing recruitment may help control chronic inflammation, autoimmune responses, or tissue damage. Because trafficking includes sequential signaling and adhesion events, treatment approaches can be considered in relation to the stage that needs adjustment.
Cancer is one of the tissue contexts in which local signals can direct immune-cell recruitment. Studying these movements helps explain how leukocytes reach tumor-associated sites and supports efforts to modify immune access. The same framework also connects cancer research with infection, injury, and inflammatory disease, where researchers must distinguish protective recruitment from infiltration that contributes to pathology.