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Updated: Dec 25, 2025

Murine Model of CD40-activation of B cells
Published on: March 5, 2010
The CD40-CD40L Dyad as Immunotherapeutic Target in Cardiovascular Disease
Laura A Bosmans1, Lena Bosch2, Pascal J H Kusters1,3
1Department of Medical Biochemistry, Amsterdam Cardiovascular Sciences (ACS), Amsterdam University Medical Centers, University of Amsterdam, Meibergdreef 15, 1105 AZ, Amsterdam, The Netherlands.
Insights
Chronic inflammation fuels atherosclerosis. Targeting the CD40-CD40L pathway offers a promising therapeutic strategy to address residual inflammatory risk in atherosclerotic cardiovascular disease.
Area of Science:
- Cardiovascular Medicine
- Immunology
- Inflammation Biology
Background:
- Chronic inflammation is a key driver of atherosclerosis.
- Residual inflammatory risk persists despite optimal cardiovascular risk factor management.
- The CD40-CD40L pathway plays a critical role in immune cell interactions during atherosclerosis development.
Purpose of the Study:
- To review the role of the CD40-CD40L dyad in atherosclerosis.
- To discuss novel therapeutic strategies targeting CD40-CD40L in cardiovascular medicine.
Main Methods:
- Literature review of the CD40-CD40L pathway in atherosclerosis.
- Analysis of recent studies on CD40-CD40L targeting strategies.
Main Results:
- The CD40-CD40L dyad is central to inflammatory responses in atherosclerosis.
- Emerging therapeutic strategies focus on modulating this pathway.
Conclusions:
- Targeting the CD40-CD40L pathway represents a potential strategy to mitigate residual inflammatory risk in atherosclerotic cardiovascular disease.
- Further research into CD40-CD40L inhibitors is warranted for cardiovascular medicine.
Abstract:
Chronic inflammation drives the development of atherosclerosis. Despite optimal treatment of classical cardiovascular risk factors, a substantial portion of the population has elevated inflammatory biomarkers and develops atherosclerosis-related complications, indicating that a residual inflammatory risk drives atherosclerotic cardiovascular disease in these patients. Additional anti-inflammatory therapeutic strategies are therefore required. The co-stimulatory molecule CD40 and its ligand CD40L (CD154) have a central role in the regulation of the inflammatory response during the development of atherosclerosis by modulating the interaction between immune cells and between immune cells and non-immune cells. In this review, we discuss the role of the CD40-CD40L dyad in atherosclerosis, and we discuss recent studies on the therapeutic potential of novel CD40-CD40L targeting strategies in cardiovascular medicine.
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