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Inflammatory Response

Inflammatory Response

An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...

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Related Experiment Video

Updated: Jan 16, 2026

Author Spotlight: Isolation and Culture of Primary Synovial Macrophages and Fibroblasts from Murine Arthritis Tissue

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Published on: February 24, 2023

Engineered Apoptotic Extracellular Vesicles for Programmable Regulation of Neutrophil-Macrophage-ROS Pathogenic Axis

Yaqing Kang^1,2, Xiaoqing Han¹, Shijie Zhou^1,2

¹State Key Laboratory of Rare Earth Resource Utilization & Laboratory of Chemical Biology, Changchun Institute of Applied Chemistry, Chinese Academy of Sciences, Changchun, 130022, China.

Advanced Materials (Deerfield Beach, Fla.)

|October 3, 2025

Summary

Engineered apoptotic extracellular vesicles (ApoEV) reprogram the rheumatoid arthritis microenvironment by targeting neutrophils and macrophages. This novel therapy reconstructs immune homeostasis and shows promise for treating rheumatoid arthritis (RA).

Keywords:

Fas/FasL signaling pathway engineered extracellular vesicles programmable regulation reconstruction rheumatoid arthritis microenvironment

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Published on: December 21, 2011

Area of Science:

Biomedical Engineering
Immunology
Nanomedicine

Background:

The rheumatoid arthritis microenvironment (RAM) involves complex interactions driving disease progression.
Current rheumatoid arthritis (RA) treatments often fail due to limited impact on the RAM.

Purpose of the Study:

To develop engineered apoptotic extracellular vesicles (ApoEV) for programmable regulation of the neutrophil-macrophage-ROS axis.
To reconstruct the RAM and enhance RA therapy.

Main Methods:

Mesenchymal stem cells (MSCs) were treated with dexamethasone (Dex) and induced apoptosis to create Dex-loaded, FasL-overexpressing ApoEV (D@ApoEV^FasL).
ApoEV were modified with low-molecular-weight heparin (LMWH) via a ROS-responsive linker, forming D@ApoEV^FasL∩L.
In vivo studies in RA mice involved intravenous injection of D@ApoEV^FasL∩L to assess joint targeting and therapeutic effects.

Main Results:

D@ApoEV^FasL∩L targeted inflamed joints and inhibited neutrophil recruitment by binding P-selectin.
High ROS levels triggered LMWH shedding, exposing FasL to induce neutrophil apoptosis via the Fas/FasL pathway.
Apoptotic neutrophils promoted M2 macrophage reprogramming, and released Dex reduced oxidative damage, restoring immune homeostasis.

Conclusions:

Engineered D@ApoEV^FasL∩L effectively regulate neutrophils, macrophages, and ROS in the RA microenvironment.
This approach triggers a beneficial immune cascade, reconstructs intra-articular immune homeostasis, and demonstrates significant therapeutic potential for RA.