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Phagocytosis of Apoptotic Cells

Phagocytosis of Apoptotic Cells

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.
Normal cells contain receptors that prevent them from being recognized...

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Related Experiment Video

Updated: Sep 23, 2025

In vitro Quantitative Imaging Assay for Phagocytosis of Dead Neuroblastoma Cells by iPSC-Macrophages

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Microglial Immunoregulation by Apoptotic Cellular Membrane Mimetic Polymeric Particles.

Yasuhiro Nakagawa^1,2,3,4,5, Jeonggyu Lee^4,5, Yihua Liu⁴

¹School of Materials and Chemical Technology, Tokyo Institute of Technology, 2-12-1 Ookayama, Meguro-ku, Tokyo 152-8550, Japan.

ACS Macro Letters

|May 16, 2022

Summary

Phosphatidylserine-exposing polymeric particles (PSPs) effectively polarize microglia from an inflammatory (Mi1) to an anti-inflammatory (Mi2) state. This suggests PSPs hold promise for novel anti-inflammatory therapies.

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Last Updated: Sep 23, 2025

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Published on: February 14, 2021

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Microglia as a Surrogate Biosensor to Determine Nanoparticle Neurotoxicity

Microglia as a Surrogate Biosensor to Determine Nanoparticle Neurotoxicity

Published on: October 25, 2016

Area of Science:

Immunology
Biomaterials Science
Neuroinflammation

Background:

Phosphatidylserine (PtdSer) is a phospholipid exposed on apoptotic cells, known to modulate immune responses.
Microglia, the resident immune cells of the central nervous system, exist in different activation states, including inflammatory (Mi1) and anti-inflammatory (Mi2) phenotypes.
Targeting microglia polarization is a key strategy for developing anti-inflammatory therapies.

Purpose of the Study:

To investigate the microglia polarization effects of PtdSer-exposing polymeric particles (PSPs).
To evaluate the therapeutic potential of PSPs in modulating neuroinflammation.

Main Methods:

In vitro cell culture experiments using microglia.
In vivo animal models to assess therapeutic efficacy.
Analysis of microglia polarization markers (Mi1 and Mi2).
Investigation of the underlying molecular mechanisms, including peroxisome proliferator-activated receptor gamma (PPARγ) signaling.

Main Results:

PSPs successfully induced a shift in microglia polarization.
Upregulation of the anti-inflammatory Mi2 microglia phenotype was observed.
Suppression of the inflammatory Mi1 microglia phenotype was achieved.
PPARγ upregulation was identified as a key mechanism mediating PSP effects both in vitro and in vivo.

Conclusions:

PSPs effectively polarize microglia towards an anti-inflammatory phenotype.
The mechanism involves the upregulation of PPARγ.
PSPs demonstrate significant potential for developing novel anti-inflammatory therapies, particularly for neuroinflammatory conditions.