Abstract
Under normal circumstances, vascular endothelium performs various functions related to homeostasis of the arterial wall, including control of vessel wall tone and vascular permeability, maintenance of blood fluidity and quiescence of inflammation [1–5]. Compromise of these activities, collectively described as endothelial dysfunction, is an important contributor to the process leading to atherosclerosis. Atherosclerotic plaques contain cellular and molecular effectors of both innate and adaptive immunity, and it is increasingly appreciated that these immune system cells play an important role in various stages of the atherosclerotic process [6–11]. In this chapter, we will focus on how the immune system can alter (“activate”), injure or otherwise impair EC functions and how these changes may contribute to atherogenesis. We will further consider how, once the process of atherogenesis has been initiated, the altered endothelium may contribute to the progression of atherosclerosis both through maintenance of a chronic inflammatory response and through modulation of the characteristics of the immune response. Finally, we will consider how impaired endothelium may contribute to the sequelae of atherosclerosis.
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Fogal, B., Pober, J.S. (2012). Vascular Endothelial Cells as Immunological Targets in Atheroscleroisis. In: Wick, G., Grundtman, C. (eds) Inflammation and Atherosclerosis. Springer, Vienna. https://doi.org/10.1007/978-3-7091-0338-8_6
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