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Related Concept Videos

Phagocytosis of Apoptotic Cells01:17

Phagocytosis of Apoptotic Cells

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Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or  immature dendritic cells. Non-professional phagocytes such as  epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes. 
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Immune Surveillance by NK Cells and Phagocytes01:25

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Immune surveillance is an integral part of the innate immune system, involving the continuous monitoring of peripheral tissues to detect and respond to pathogens, infected cells, or cancerous cells. This surveillance is conducted primarily by natural killer (NK) cells and phagocytes, which employ distinct but complementary mechanisms to identify and eliminate threats.
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Phagocytosis00:41

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Cells pull particles inward and engulf them in spherical vesicles in an energy-requiring process called endocytosis. Phagocytosis (“cellular eating”) is one of three major types of endocytosis. Cells use phagocytosis to take in large objects—such as other cells (or their debris), bacteria, and even viruses.
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Cells pull particles inward and engulf them in spherical vesicles in an energy-requiring process called endocytosis. Phagocytosis ("cellular eating") is one of three major types of endocytosis. Cells use phagocytosis to take in large objects, such as other cells (or their debris), bacteria, and even viruses.
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Receptor-mediated Endocytosis01:39

Receptor-mediated Endocytosis

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Overview
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Receptor-mediated Endocytosis01:20

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Receptor-mediated endocytosis is when bulk amounts of specific molecules are imported into a cell after binding to cell surface receptors. The molecules bound to these receptors are taken into the cell through inward folding of the cell surface membrane, which is eventually pinched off into a vesicle within the cell. Structural proteins, such as clathrin, coat the budding vesicle.
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Related Experiment Video

Updated: Nov 1, 2025

"Phagosome Closure Assay" to Visualize Phagosome Formation in Three Dimensions Using Total Internal Reflection Fluorescent Microscopy TIRFM
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"Phagosome Closure Assay" to Visualize Phagosome Formation in Three Dimensions Using Total Internal Reflection Fluorescent Microscopy TIRFM

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Pro-Resolving Ligands Orchestrate Phagocytosis.

Christa Decker1, Sudeshna Sadhu1, Gabrielle Fredman1

  • 1The Department of Molecular and Cellular Physiology, Albany Medical College, Albany, NY, United States.

Frontiers in Immunology
|June 28, 2021
PubMed
Summary
This summary is machine-generated.

Specialized pro-resolving mediators (SPMs) enhance the resolution of inflammation by improving phagocytosis and efferocytosis. Understanding these mechanisms is crucial for treating diseases linked to failed inflammation resolution.

Keywords:
efferocytosisinflammationmacrophagephagocytosisresolvin

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Area of Science:

  • Biomedical Science
  • Immunology
  • Molecular Biology

Background:

  • Inflammation resolution is a vital tissue-protective process.
  • Specialized pro-resolving mediators (SPMs), proteins, gases, and nucleotides regulate inflammation.
  • Phagocytes, such as neutrophils and macrophages, are critical for clearing debris and dead cells via phagocytosis and efferocytosis.

Purpose of the Study:

  • To review the mechanisms by which SPMs enhance phagocytosis and efferocytosis.
  • To highlight the importance of understanding these processes for human health.

Main Methods:

  • Literature review of existing research on inflammation resolution and SPMs.
  • Analysis of the roles of phagocytosis and efferocytosis in disease.

Main Results:

  • SPMs are key regulators that promote the resolution of inflammation.
  • SPMs enhance the function of phagocytes, improving debris and dead cell clearance.
  • Defective inflammation resolution and phagocytosis are implicated in prevalent human diseases.

Conclusions:

  • Targeting SPMs offers a potential therapeutic strategy for diseases associated with failed inflammation resolution.
  • Further research into SPM mechanisms can lead to novel treatments for inflammatory conditions.