Leukocyte Recruitment
Leukocyte Recruitment - Related Videos
11:30
Analyzing the Effects of Stromal Cells on the Recruitment of Leukocytes from Flow
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Cited by 28 •
2015
The ability of inflamed endothelium to recruit leukocytes from flow is regulated by mesenchymal stromal cells. We describe two in vitro models incorporating primary human cells that can be used to assess neutrophil recruitment from flow and examine the role that mesenchymal stromal cells play in regulating this process.
05:52
An In Vitro Flow Investigation of the Effect of Stromal Cells on Leukocyte Recruitment
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2025
The video demonstrates a method for investigating the impact of stromal cells on leukocyte recruitment. In a parallel plate flow chamber model, pro-inflammatory cytokines induce the expression of adhesion receptors by endothelial cells, facilitating neutrophil recruitment and migration. The cross-talk between stromal cells and endothelial cells diminishes neutrophil recruitment to the endothelial cells.
07:50
Multiphoton Intravital Imaging for Monitoring Leukocyte Recruitment during Arteriogenesis in a Murine Hindlimb Model
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Cited by 1 •
2021
The recruitment of leukocytes and platelets constitutes an essential component necessary for the effective growth of collateral arteries during arteriogenesis. Multiphoton microscopy is an efficient tool for tracking cell dynamics with high spatio-temporal resolution in vivo and less photo-toxicity to study leukocyte recruitment and extravasation during arteriogenesis.
07:42
Non-invasive Imaging of Leukocyte Homing and Migration in vivo
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Cited by 8 •
2010
Here, we describe a non-invasive two-photon (2P) microscopy approach to study leukocyte homing in the mouse footpad. We discuss the technical aspects of our tissue imaging preparation and walk the reader through a typical experiment from initial set up to execution and data collection.
03:42
Isolation of Marginating Hepatic Leukocytes from a Mouse Liver
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2025
In this video, we demonstrate the isolation of marginating hepatic leukocytes from mouse liver by forced perfusion.
FAQs
Selectins provide the initial, transient contacts that slow circulating leukocytes and produce rolling along the vessel surface. Inflammatory signals then activate leukocyte integrins, enabling firmer attachment to the endothelium. This staged transition matters because cells must first be captured from flowing blood and then retained long enough to cross the vessel wall rather than continue circulating.
Chemokine gradients provide directional information once leukocytes have crossed the vessel wall. Cells follow increasing chemokine signals toward the affected tissue, concentrating their movement where infection, injury, or another immune stimulus is strongest. This guidance makes recruitment spatially organized rather than random and helps position responding cells at the site requiring immune activity.
Endothelial activation converts the vessel lining from a relatively passive barrier into a surface that can engage leukocytes. Inflammatory mediators induce the interactions needed for tethering, rolling, and subsequent firm adhesion. Because this response controls when and where circulating cells can exit, endothelial activation helps target recruitment to affected tissue instead of producing indiscriminate accumulation.
Diapedesis is the passage of an adherent leukocyte across the vessel wall into surrounding tissue. It represents the transition from vascular positioning to tissue access, allowing the cell to respond locally rather than remaining attached to the endothelial surface. In infection and injury, this step is necessary for recruited leukocytes to reach signals and targets beyond the bloodstream.
During infection, recruitment coordinates different layers of host defense. Incoming leukocytes contribute to innate responses that act against pathogens, while the broader process also helps coordinate adaptive immune activity. Its value therefore extends beyond bringing cells to an inflamed site: it links vascular signals with pathogen elimination and the organized deployment of immune protection.
When recruitment is excessive or misdirected, the same traffic-control system that supports defense can contribute to chronic inflammation, tissue damage, and immune-mediated disease. The problem is not simply leukocyte presence, but inappropriate magnitude or location of accumulation. This makes regulation of endothelial activation, adhesion, tissue entry, and chemokine-guided positioning important for limiting collateral injury.
Leukocyte recruitment also participates in tissue repair after injury. By directing immune cells into affected tissue, it helps connect the early response to processes that restore damaged sites. This dual role explains why recruitment can be beneficial when appropriately localized yet harmful when prolonged or misdirected, with outcomes ranging from repair support to ongoing tissue injury.