Related Experiment Video
Updated: Aug 9, 2026
In Vitro and In Vivo Assessment of T, B and Myeloid Cells Suppressive Activity and Humoral Responses from Transplant Recipients
Published on: August 12, 2017
T cell costimulation in the development of cardiac allograft vasculopathy: potential targets for therapeutic
Mitsuaki Isobe1, Hisanori Kosuge, Jun-Ichi Suzuki
1Department of Cardiovascular Medicine, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyoku, Tokyo 113-8519, Japan. isobemi.cvm@tmd.ac.jp
Insights
Cardiac allograft vasculopathy (CAV) involves arterial stenosis after heart transplants. Targeting costimulatory pathways may treat CAV and atherosclerosis by modulating T cell activation and inflammation.
Area of Science:
- Immunology and Transplantation Biology
- Cardiovascular Pathology and Atherosclerosis Research
Background:
- Cardiac allograft vasculopathy (CAV) is a major cause of late mortality post-heart transplantation, characterized by arterial stenosis.
- The pathology involves diffuse intimal hyperplasia and inflammatory cell infiltration, particularly T cells, in the arterial wall.
- Endothelial cell damage triggers inflammatory responses and T cell activation, crucial for CAV development.
Purpose of the Study:
- To review the current understanding of costimulatory pathways in the pathogenesis of CAV.
- To explore the potential of targeting these pathways for therapeutic interventions in CAV and atherosclerosis.
Main Methods:
- Literature review summarizing existing research on costimulatory molecules and their role in CAV.
- Analysis of the involvement of specific costimulatory pathways in T cell activation within the context of allograft vasculopathy and atherosclerosis.
Main Results:
- Several costimulatory pathways are implicated in the development of CAV and general atherogenesis.
- These pathways are critical for T cell activation, contributing to the inflammatory processes underlying CAV.
Conclusions:
- Understanding the role of costimulatory pathways provides insights into CAV pathogenesis.
- Modulating these pathways presents a potential therapeutic strategy for treating heart allograft vascular disease and atherosclerosis.
Abstract:
Cardiac allograft vasculopathy (CAV) is a form of coronary arterial stenosis and a leading cause of death in patients who survive beyond the first year after heart transplantation. Histopathologically, this lesion is concentric diffuse intimal hyperplasia of the arterial wall that is accompanied by extensive infiltration of inflammatory cells, including T cells. Many studies have explored the potential risk factors related to this arterial lesion and its pathogenesis. Continuous minor endothelial cell damage evokes inflammatory processes including T cell activation. Costimulatory molecules play crucial roles in this T cell activation. Many costimulatory pathways have been described, and some are involved in the pathogenesis of CAV, atherogenesis, and subsequent plaque formation. In this review, we summarize the present knowledge of the role of these pathways in CAV development and the possibility of manipulating these pathways as a means to treat heart allograft vascular disease and atherosclerosis.
