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The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
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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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Related Experiment Video

Updated: Sep 17, 2025

Saturated Fatty Acids Induce Ceramide-associated Macrophage Cell Death
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M1 Macrophage-Derived Extracellular Particles Induce Cell Death in MDA-MB-231 Cells.

Parth Desai1, Anjali Kumari2, Saqer Al Abdullah2

  • 1Department of Nanoscience, Joint School of Nanoscience and Nanoengineering, University of North Carolina at Greensboro, Greensboro, North Carolina, USA.

Cancer Reports (Hoboken, N.J.)
|July 2, 2025
PubMed
Summary
This summary is machine-generated.

Extracellular particles (EPs) from M1 macrophages induce cell death in triple-negative breast cancer (TNBC) cells. This finding suggests macrophage-derived EPs could offer novel therapeutic strategies for TNBC treatment.

Keywords:
caspasecytotoxicityextracellular particlesmacrophagetriple‐negative breast cancer

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Detection of Inflammasome Activation and Pyroptotic Cell Death in Murine Bone Marrow-derived Macrophages
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Area of Science:

  • Immunology
  • Cancer Biology
  • Cell Biology

Background:

  • Triple-negative breast cancer (TNBC) is a deadly disease with limited treatment options.
  • Macrophages play a key role in immune responses and can secrete extracellular particles (EPs).
  • EPs are involved in intercellular communication and immune modulation, suggesting potential therapeutic roles.

Purpose of the Study:

  • To investigate the therapeutic potential of M1 macrophage-secreted EPs against TNBC.
  • To examine the effects of M1 EPs on TNBC cell viability and death.

Main Methods:

  • RAW 264.7 macrophages were polarized to M1 phenotype.
  • Macrophage-derived EPs were isolated and characterized using nanoparticle tracking analysis, electron microscopy, and western blotting.
  • The impact of M1 EPs on MDA-MB-231 (TNBC) cells was assessed via confocal microscopy, observing caspase 3/7 expression and cell death.

Main Results:

  • M1 macrophage-derived EPs were successfully isolated and characterized.
  • Exposure to M1 EPs led to a time-dependent increase in caspase 3/7 expression in TNBC cells.
  • M1 EPs induced cell death in TNBC cells, whereas M2 EPs promoted proliferation.

Conclusions:

  • EPs derived from M1 macrophages demonstrate a capacity to induce cell death in TNBC cells.
  • These findings highlight the potential of M1 macrophage-derived EPs as a novel therapeutic approach for TNBC.