Infected Erythrocyte Exposure
Infected Erythrocyte Exposure - Related Videos
06:56
An Assay for Quantifying Antibody-Mediated Phagocytosis of Parasite-Infected Erythrocytes
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2025
This video demonstrates a flow cytometry-based phagocytosis assay involving labeled and opsonized Plasmodium falciparum-infected erythrocytes by monocytes. Flow cytometry identifies fluorescence in monocytes, confirming the successful identification of opsonized erythrocytes through phagocytosis.
05:20
Separation of Plasmodium falciparum Late Stage-infected Erythrocytes by Magnetic Means
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Cited by 7 •
2013
The paramagnetic properties of hemozoin are used to isolate late stages of Plasmodium falciparum-infected red blood cells growing in culture. The method is simple and fast and does not affect the subsequent invasive capabilities of the parasites.
07:27
A Simple Protocol for Platelet-mediated Clumping of Plasmodium falciparum-infected Erythrocytes in a Resource Poor Setting
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2013
This method investigates the platelet-mediated clumping phenotype of Plasmodium falciparum-infected erythrocytes (pRBC) in clinical isolates. This is performed by isolating and co-incubating platelet-rich plasma and a suspension of pRBC.
01:22
Lifecycle of Erythrocytes
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2024
Erythrocytes, also known as red blood cells, constantly move through blood capillaries. As a result, they damage their plasma membrane due to the continuous friction. Typically, after 100 to 120 days, erythrocytes become rigid and fragile as they wear out. As they pass through small vessels in the spleen and liver, they can get trapped and break apart into fragments. The resident phagocytic macrophages deal with these damaged cells by engulfing them and separating their globin and heme groups.
01:27
Disorders of Erythrocytes
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2024
Disorders of erythrocytes, or red blood cells (RBCs), include a range of conditions affecting their number, shape, or function. Erythrocyte disorders can be broadly categorized into two main types: anemic and polycythemic conditions. A low oxygen-carrying capacity of the blood due to the loss, lower production, or destruction of erythrocytes is termed anemia. Hemorrhagic anemia, for example, occurs when bleeding from an external wound or internal ulcer reduces erythrocyte counts. On the other...
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Two signal sources can operate during exposure: physical contact between immune cells and infected erythrocytes, and molecules released or displayed by the intracellular pathogen. Together, they may activate innate immune signaling and influence whether cells phagocytose targets, process pathogen-associated antigens, or release inflammatory mediators. Separating these contributions helps clarify how host cells detect blood-stage infection.
The responding immune cell type can determine which effects are most evident, including recognition, phagocytosis, antigen processing, or cytokine release. Experimental conditions also modify these outcomes, so identical infected erythrocytes may produce different response profiles in different cellular settings. This comparison helps identify cell-specific mechanisms of host defense and reveals which immune functions contribute to pathogen control.
Cytokine release indicates that immune cells have detected and responded to the exposure, while phagocytosis shows a cellular clearance activity directed toward infected erythrocytes. Examining these readouts together distinguishes inflammatory signaling from physical uptake of targets. Their patterns can therefore reveal whether a response favors immune activation, pathogen removal, or potential immune evasion.
A basic workflow brings immune cells into contact with erythrocytes harboring the intracellular pathogen, maintains the selected experimental conditions, and then assesses cellular and secreted responses. Researchers can examine recognition-associated signaling, phagocytosis, antigen processing, and inflammatory mediator release. Organizing measurements around these outcomes connects the exposure event with specific mechanisms of host response.
The approach can show whether immune cells recognize infected erythrocytes, initiate uptake, process pathogen-derived antigens, or produce inflammatory mediators. A strong clearance-associated response may point to effective cellular control, whereas limited or altered responses can help identify possible immune-evasion mechanisms. Interpreting these outcomes together provides a cellular view of blood-stage infection biology.
Researchers apply this model to characterize host responses to blood-stage infection and to evaluate interventions that may alter those responses. It can support investigation of vaccine effects, therapeutic strategies, and host-directed interventions by measuring immune recognition, cytokine responses, antigen processing, and pathogen-clearance mechanisms. These results help connect cellular observations with disease mechanisms and intervention priorities.