Monocyte Monolayer
Monocyte Monolayer - Related Videos
03:30
An Assay for Studying Fcγ Receptor-Driven Phagocytosis in Monocyte Monolayers
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2025
This video showcases a monocyte monolayer assay utilizing primary monocytes from peripheral blood to assess Fcγ receptor-mediated phagocytosis with poly D antibody-opsonized R2R2 red blood cells.
06:27
Use of a Monocyte Monolayer Assay to Evaluate Fcγ Receptor-mediated Phagocytosis
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Cited by 13 •
2017
The monocyte monolayer assay (MMA) is an in vitro assay that utilizes isolated primary monocytes obtained from mammalian peripheral whole blood to evaluate Fcγ receptor (FcγR)-mediated phagocytosis.
08:31
Characterization of Human Monocyte-derived Dendritic Cells by Imaging Flow Cytometry: A Comparison between Two Monocyte Isolation Protocols
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Cited by 19 •
2016
This study compares two different methods of human monocyte isolation for obtaining in vitro dendritic cells (DCs). Monocytes are selected by adherence or negatively enriched by magnetic separation. Monocyte yield and viability along with MDDC viability, proliferation and CD11c/CD14 surface marker expression will be compared between both methods.
04:27
Isolation of Monocytes from Whole Blood by Immunomagnetic Negative Selection
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2025
In this video, we demonstrate the isolation of monocytes from whole human blood by immunomagnetic negative separation. The isolated monocytes can be used for further downstream analysis.
03:05
In Vitro Culture and Differentiation of Primary Monocytes into Macrophages
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2025
This video demonstrates the priming of primary monocytes into macrophages. Primary human monocytes can be isolated and differentiated to an M1-like pro-inflammatory phenotype using the granulocyte-macrophage colony-stimulating factor (GM-CSF) or to an M2-like anti-inflammatory phenotype using the macrophage colony-stimulating factor (M-CSF).
FAQs
Adhesion to the culture surface is mediated by cell-surface adhesion molecules, establishing the attached cell layer needed for observation and treatment. Subsequent exposure to cytokines or pathogen-associated molecular patterns can activate the cells, producing changes in morphology, gene expression, and cytokine release. These linked responses allow investigators to connect environmental stimuli with measurable innate immune outcomes.
These stimuli model distinct types of immune activation within a controlled system. Cytokines can alter monocyte behavior through inflammatory signaling, whereas pathogen-associated molecular patterns mimic molecular cues associated with microbes. Comparing the resulting morphology, gene-expression changes, and cytokine release helps researchers examine how monocytes recognize or respond to inflammatory and infection-related conditions.
Differentiation toward macrophage-like cells represents a change in monocyte state that can follow activation in culture. This transition provides a way to study how innate immune cells alter their behavior over time, including changes in morphology, inflammatory output, and functional responses such as phagocytic activity. It also helps connect early monocyte responses with later immune-cell behavior.
Several complementary outcomes can be examined: visible morphological changes, altered gene expression, cytokine release, phagocytic activity, and differentiation toward macrophage-like cells. Together, these measurements capture both cellular state and immune function rather than relying on a single indicator. The combination can reveal whether a microbial stimulus or treatment changes inflammatory signaling and host-cell activity.
Preparation begins by establishing monocytes on a culture surface where cell-surface adhesion molecules support attachment and formation of the layer. The attached cells can then be exposed to selected cytokines, pathogen-associated molecular patterns, microbial stimuli, or treatments, followed by assessment of cellular and immune responses. This controlled sequence supports comparisons between stimulated, treated, and otherwise different experimental conditions.
The model is useful when researchers need a simplified, controlled system for examining host-pathogen interactions, inflammatory signaling, phagocytic activity, or immune-cell behavior. It can compare monocyte responses to different microbial stimuli and test whether treatments modify inflammation. Findings from the monolayer can complement studies in complex tissues or whole-animal systems without replacing those broader contexts.