• Simeng Tian, Yufei Wang, Jie Wan, Mao Yang, and Zhenkun Fu.
• Department of Immunology, Basic Medicine College, Heilongjiang Provincial Key Laboratory for Infection and Immunity, Harbin Medical University, Heilongjiang Academy of Medical Science, Harbin, China.
• Medicine (Baltimore). 2024 Apr 5; 103 (14): e37718e37718.

AbstractThe interaction between CD40 and CD40 ligand (CD40L) a crucial co-stimulatory signal for activating adaptive immune cells, has a noteworthy role in atherosclerosis. It is well-known that atherosclerosis is linked to immune inflammation in blood vessels. In atherosclerotic lesions, there is a multitude of proinflammatory cytokines, adhesion molecules, and collagen, as well as smooth muscle cells, macrophages, and T lymphocytes, particularly the binding of CD40 and CD40L. Therefore, research on inhibiting the CD40-CD40L system to prevent atherosclerosis has been ongoing for more than 30 years. However, it's essential to note that long-term direct suppression of CD40 or CD40L could potentially result in immunosuppression, emphasizing the critical role of the CD40-CD40L system in atherosclerosis. Thus, specifically targeting the CD40-CD40L interaction on particular cell types or their downstream signaling pathways may be a robust strategy for mitigating atherosclerosis, reducing potential side effects. This review aims to summarize the potential utility of the CD40-CD40L system as a viable therapeutic target for atherosclerosis.Copyright © 2024 the Author(s). Published by Wolters Kluwer Health, Inc.

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