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Arteriosclerosis, Thrombosis, and Vascular Biology
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Published Online
on April 20, 2006

Arteriosclerosis, Thrombosis, and Vascular Biology. 2006
Published online before print April 20, 2006, doi: 10.1161/01.ATV.0000222906.78307.7b
A more recent version of this article appeared on July 1, 2006
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Submitted on October 31, 2005
Accepted on March 2, 2006

T Cell Costimulation in the Development of Cardiac Allograft Vasculopathy. Potential Targets for Therapeutic Interventions

Mitsuaki Isobe *; Hisanori Kosuge ; and Jun-ichi Suzuki

From the Department of Cardiovascular Medicine, Tokyo Medical and Dental University, Tokyo, Japan.

* To whom correspondence should be addressed. E-mail: isobemi.cvm{at}tmd.ac.jp.

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.




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