Cardiac Disease: Exploration of Atherosclerosis's Impact on the Immune System
A new study, published in the prestigious journal Nature Communications, is exploring a promising drug target for the suppression of atherosclerosis. The research, led by immunologists and cardiovascular scientists, focuses on the interaction between CD40L and CD40 proteins.
Atherosclerosis, one of the most common causes of death in Germany, results in the build-up of cholesterol and other fatty metabolites in the arterial wall, leading to the constriction of the artery and the obstructing of blood flow. This can trigger heart attacks and strokes.
Statins, a commonly used drug for treating atherosclerosis, effectively reduce the risk of cardiovascular disease in only 35 to 40% of the patients treated. The remaining 60% fail to respond to statin medication, highlighting the need for alternative treatment options.
The research by Lutgens' group suggests that deletion of CD40L in T-cells and dendritic cells reduces the size and instability of atherosclerotic plaques. This could enhance plaque stability and reduce the risk of heart attacks.
The interaction between CD40L and CD40 proteins occurs when CD40L, synthesized by specialized cells of the immune system, is recognized by the CD40 protein on antigen-presenting cells. Lutgens' team's research provides evidence for differential, cell-type-specific functions of the CD40L/CD40 interaction in atherosclerosis.
The researchers propose that this could be achieved using small-molecule inhibitors or bifunctional antibodies with different binding sites. This approach could potentially inhibit the functions of these proteins in a cell-specific fashion, making it a promising avenue for future drug development.
Immunotherapy is being explored as a potential treatment for atherosclerosis, with recent studies verifying the key role of T cells and specific cytokines in the immune response associated with atherosclerosis. By selectively inhibiting these immune pathways, researchers have observed reduced plaque formation and inflammation in mouse models.
The DOI for the study is 10.1038/s41467-021-23909-z. This research offers a significant step forward in understanding the role of the CD40L/CD40 interaction in atherosclerosis and could pave the way for new therapeutic strategies that focus on this signaling pathway.
