Related Experiment Video
Updated: Mar 23, 2026

Isolation Protocol of Mouse Monocyte-derived Dendritic Cells and Their Subsequent In Vitro Activation with Tumor Immune Complexes
Published on: May 31, 2018
CD97/ADGRE5 Inhibits LPS Induced NF-κB Activation through PPAR-γ Upregulation in Macrophages
Shuai Wang1, Zewei Sun1, Wenting Zhao1
1Department of Cardiology, First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310000, China.
Abstract:
CD97/ADGRE5 protein is predominantly expressed on leukocytes and belongs to the EGF-TM7 receptors family. It mediates granulocytes accumulation in the inflammatory tissues and is involved in firm adhesion of PMNC on activated endothelial cells. There have not been any studies exploring the role of CD97 in LPS induced NF-κB activation in macrophages. Therefore, we first measured the CD97 expression in LPS treated human primary macrophages and subsequently analyzed the levels of inflammatory factor TNF-α and transcription factor NF-κB in these macrophages that have been manipulated with either CD97 knockdown or overexpression. We found that a reported anti-inflammatory transcription factor, PPAR-γ, was involved in the CD97 mediated NF-κB suppression. Furthermore, by immunofluorescence staining, we established that CD97 overexpression not only inhibited LPS induced p65 expression in the nucleus but also promoted the PPAR-γ expression. Moreover, using CD97 knockout THP-1 cells, we further demonstrated that CD97 promoted PPAR-γ expression and decreased LPS induced NF-κB activation. In conclusion, CD97 plays a negative role in LPS induced NF-κB activation and TNF-α secretion, partly through PPAR-γ upregulation.
Insights
CD97 protein suppresses lipopolysaccharide (LPS)-induced NF-κB activation and TNF-α secretion in macrophages, partly by upregulating the anti-inflammatory transcription factor PPAR-γ.
Area of Science:
- Immunology
- Cell Biology
- Molecular Biology
Background:
- CD97/ADGRE5, an EGF-TM7 receptor family member, is expressed on leukocytes and influences inflammatory responses.
- Its role in lipopolysaccharide (LPS)-induced nuclear factor-kappa B (NF-κB) activation in macrophages remains unexplored.
Purpose of the Study:
- To investigate the role of CD97 in LPS-induced NF-κB activation and inflammatory factor production in macrophages.
- To elucidate the involvement of PPAR-γ in CD97-mediated regulation of NF-κB signaling.
Main Methods:
- Assessed CD97 expression in LPS-treated human primary macrophages.
- Manipulated CD97 levels (knockdown/overexpression) and analyzed NF-κB and TNF-α.
- Utilized immunofluorescence staining to examine p65 and PPAR-γ expression.
- Employed CD97 knockout THP-1 cells to confirm findings.
Main Results:
- CD97 overexpression inhibited LPS-induced p65 nuclear translocation and TNF-α secretion.
- CD97 manipulation affected PPAR-γ expression, suggesting its involvement in the pathway.
- CD97 knockout cells showed decreased LPS-induced NF-κB activation.
- CD97 was found to promote PPAR-γ expression.
Conclusions:
- CD97 negatively regulates LPS-induced NF-κB activation and TNF-α secretion in macrophages.
- This suppression is partly mediated by the upregulation of PPAR-γ.
- CD97 plays a crucial role in modulating inflammatory responses in macrophages.
More Related Videos
Related Concept Videos
NF-κB-dependent Signaling Pathway
NF-κB-dependent Signaling Mechanism
The...
NF-kB-dependent Signaling Pathway
Co-activators and Co-repressors

