The multi-functionality of CD40L and its receptor CD40 in atherosclerosis
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Updated: Jun 21, 2026

Murine Model of CD40-activation of B cells
Published on: March 5, 2010
Dirk Lievens1, Wouter J Eijgelaar, Erik A L Biessen
1Department of Pathology, University of Maastricht, 6229 HX Maastricht, The Netherlands.
Insights
Inhibiting the CD40-CD40L pathway stabilizes atherosclerotic plaques by reducing inflammation. Targeted inhibition strategies are needed to avoid compromising immune defense for effective atherosclerosis treatment.
Area of Science:
- Cardiovascular Biology
- Immunology
- Molecular Medicine
Background:
- The CD40-CD40L pathway plays a crucial role in immune responses and is implicated in atherosclerosis.
- Disruption of this pathway leads to a more stable atherosclerotic plaque phenotype, characterized by reduced inflammation and increased fibrosis.
- CD40 and CD40L are expressed on various cells within the plaque, including macrophages, endothelial cells, and vascular smooth muscle cells, contributing to atherogenesis.
Purpose of the Study:
- To review the cell-type specific roles of CD40-CD40L signaling in atherosclerosis.
- To highlight the potential of targeted inhibition strategies for treating atherosclerosis.
- To explore how understanding cell-cell CD40-CD40L interactions can lead to treatments that do not compromise the immune system.
Main Methods:
- Literature review focusing on CD40-CD40L interactions in atherosclerosis.
- Analysis of the multi-functionality of CD40-CD40L signaling across different cell types.
- Synthesis of current research on targeted intervention strategies.
Main Results:
- CD40-CD40L pathway disruption reduces atherosclerosis and promotes plaque stability.
- CD40 and CD40L are involved in atherogenesis through interactions on T-cells, antigen-presenting cells, macrophages, endothelial cells, vascular smooth muscle cells, neutrophils, and platelets.
- Systemic inhibition of CD40-CD40L compromises host defense.
Conclusions:
- Targeted inhibition of cell-type specific CD40-CD40L signaling components offers a promising therapeutic approach for atherosclerosis.
- Further research into cell-cell CD40-CD40L interactions is essential for developing superior, immune-sparing treatment strategies.
- Understanding the nuanced roles of CD40-CD40L signaling in different cell types is key to advancing atherosclerosis therapy.
Abstract:
Disrupting the CD40-CD40L co-stimulatory pathway reduces atherosclerosis and induces a stable atherosclerotic plaque phenotype that is low in inflammation and high in fibrosis. Therefore, inhibition of the CD40-CD40L pathway is an attractive therapeutic target to reduce clinical complications of atherosclerosis. The CD40-CD40L dyad is known to interact with other co-stimulatory molecules, to activate antigen-presenting cells (APC) and to contribute to T-cell priming and B-cell isotype switching. Besides their presence on T-cells and APCs, CD40 and CD40L are also present on macrophages, endothelial cells and vascular smooth muscle cells in the plaque, where they can exert pro-atherogenic functions. Moreover, recent progress indicates the involvement of neutrophil CD40, platelet CD40L and dendritic cell CD40 in atherogenesis. Since systemic CD40-CD40L modulation compromises host defense, more targeted interventions are needed to develop superior treatment strategies for atherosclerosis. We believe that by unravelling the cell-cell CD40-CD40L interactions, inhibition of cell-type specific (signalling components of) CD40(L) that do not compromise the patient's immune system, will become possible. In this review, we highlight the cell-type specific multi-functionality of CD40-CD40L signalling in atherosclerosis.
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