Immune Cell Recruitment
Immune Cell 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.
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.
04:28
Lung Tumor Cell Recruitment Assay
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2019
This manuscript describes a method to quantify tumor cell accumulation in the lungs in an animal model of tumor metastasis.
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.
11:38
A Flow Adhesion Assay to Study Leucocyte Recruitment to Human Hepatic Sinusoidal Endothelium Under Conditions of Shear Stress
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Cited by 31 •
2014
Leucocyte recruitment to the liver occurs within the specialized channels of the hepatic sinusoids which are lined by unique hepatic sinusoidal endothelial cells. Phase contrast microscopy of leucocyte recruitment across human hepatic sinusoidal endothelium under conditions of physiological shear stress can facilitate the elucidation of the molecular mechanisms which underlie this process.
FAQs
Entry depends on a coordinated sequence rather than chemotactic guidance alone. Signals from cancer cells, stromal cells, or blood vessels activate the endothelium, the vessel lining. Activated endothelial cells promote leukocyte adhesion, allowing circulating cells to attach to the vessel wall and then move into tumor tissue along chemotactic signals. Each step can influence how many cells reach the tumor microenvironment.
Cytokines and chemokines provide localized instructions that influence both vascular activation and leukocyte movement. Cytokines can help activate the endothelium, while chemokines guide cells through chemotaxis toward the tumor. Because several tumor-associated cell types can produce these signals, their combined activity helps determine which immune populations enter the microenvironment and where they accumulate.
The effect depends on which immune populations are recruited and how they function within the tumor microenvironment. T cells may attack malignant cells, whereas macrophages or neutrophils may, in some settings, support tumor growth, immune suppression, or metastasis. Consequently, measuring cell abundance alone may be insufficient; researchers also need to interpret the biological role associated with each recruited population.
Signals produced by cancer cells, stromal cells, and blood vessels can shape the composition and behavior of incoming leukocytes. A signaling environment that favors effective T-cell access may support antitumor activity, while recruitment associated with macrophages or neutrophils can contribute to immune suppression, growth, or metastatic processes. This context makes trafficking patterns important for understanding variable tumor behavior and treatment resistance.
Researchers examine which immune populations enter tumors and how their distribution relates to tumor biology. These trafficking patterns can help identify biomarkers, meaning measurable features associated with a biological state or response. They also provide a framework for studying why treatment resistance occurs and for determining whether inadequate immune-cell access contributes to poor antitumor activity.
Analysis of leukocyte trafficking can connect cellular localization with tumor progression, immune suppression, metastasis, or antitumor responses. It may reveal whether tumors attract populations capable of attacking malignant cells or instead create conditions that favor tumor-supportive immune activity. Such information can guide biomarker discovery and clarify how the tumor microenvironment influences treatment response.
The same general trafficking principles are relevant to inflammation and infection, where localized signals direct immune cells from circulation into affected tissues. Cancer research applies this framework to a tumor setting, in which recruited cells may either provide immune attack or support malignant progression. Comparing these contexts helps researchers distinguish shared recruitment mechanisms from tumor-specific consequences.
Recruitment biology can inform strategies designed to improve immune-cell access to tumors or redirect incoming populations toward antitumor responses. The goal is not simply to increase leukocyte entry, because some recruited cells may support immune suppression, tumor growth, or metastasis. Understanding the signals, endothelial steps, and cell types involved therefore helps define more selective therapeutic approaches.