The CD163-expressing macrophages recognize and internalize TWEAK: potential consequences in atherosclerosis

Area of Science:

• Cardiovascular Biology
• Immunology
• Biomarker Discovery

Background:

• CD163 acts as a scavenger receptor for Tumor necrosis factor-like weak inducer of apoptosis (TWEAK).
• TWEAK signaling is implicated in various biological processes relevant to atherosclerosis.

Purpose of the Study:

• To investigate the significance of the TWEAK-CD163 interaction in the context of atherosclerosis.
• To explore the potential of this interaction as a biomarker for atherosclerotic disease.

Main Methods:

• Studied TWEAK-CD163 interaction in cultured human macrophages.
• Analyzed TWEAK and CD163 expression in carotid atherosclerotic plaques and plasma.
• Assessed the association with intima-media thickness (IMT) in asymptomatic individuals.

Main Results:

• CD163-expressing macrophages internalized TWEAK in vitro.
• Observed an inverse correlation between CD163 and TWEAK expression in atherosclerotic plaques and plasma.
• Found a positive correlation between soluble CD163 (sCD163), the sCD163-TWEAK ratio, and IMT, which remained significant after adjusting for risk factors.

Conclusions:

• TWEAK-CD163 interaction occurs in vivo, potentially reducing TWEAK plasma levels.
• The CD163-TWEAK plasma ratio may serve as a valuable biomarker for clinical and subclinical atherosclerosis.