Author(s): Xu X, Lin H, Lv H, Zhang M, Zhang Y
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Abstract Arterial inflammation is a significant component of atherosclerotic disease-specific immune responses directed against autoantigens or pathogen-derived antigens in the vascular wall could initiate and/or maintain atherosclerotic processes. Atherosclerosis is now regarded as a chronic inflammatory disease. Developing in response to injury in the vessel wall, it is characterized by the infiltration of mononuclear lymphocytes into the intima, local expansion of vascular smooth muscle cells, and accumulation of extracellular matrix. A number of potential mechanisms have been implicated in the development of inflammatory reactions in the vascular system. Adventitia provides cells and molecules with the ability to influence neointimal formation and vascular remodeling implemented in part by vasa vasorum. We hypothesize that lymphatic vessels, existing in adventitia in the atherosclerotic artery, could drain local inflammatory cells and cytokines to the lymphatic nodes and lymphoid tissues where inflammatory cells can be sensitized and activated. Or, blood vessels may deliver sensitized inflammatory cells and cytokines to the inflammatory site of the vascular wall. Therefore, both lymphatic and blood vessels constitute a complete circle of immune response, whereby the inflammatory cells and cytokines are effectively delivered to tissues and their effects magnified. Under certain circumstances, this situation may lead to a vicious circle of inflammation such as in atherosclerosis, resulting in perpetuating intimal hyperplasia and vascular remodeling. Inhibition of lymphangiogenesis may interrupt this self-perpetuating vicious circle of inflammation in atherosclerosis and provide a new approach to the prevention and treatment of the disease.
This article was published in Med Hypotheses
and referenced in Journal of Clinical & Cellular Immunology