Are red blood cells part of the immune system copy to clipboard
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Atherosclerosis is a chronic inflammatory disease of the arterial wall and the leading cause of mortality in the western world [1]. Research over recent years has delineated atherosclerosis as a multifactorial disease because several factors such as hyperlipidemia, hypertension, diabetes mellitus, male gender, obesity, and family history of cardiovascular disease are implicated. Many of these factors promote mechanisms of inflammation and oxidative stress, which are both major characteristics of atherosclerosis which starts as a “response to injury” favoring immune system activation and endothelial dysfunction [1, 2]. Immune system, with elements of both innate and adaptive immunity, contributes positively and negatively to the development of complex atherosclerotic plaques. Plaque macrophages, dendritic cells (DCs), and activated T and B lymphocytes represent the majority of leukocytes in the atherosclerotic lesions and their secretory activity, including proinflammatory cytokine and matrix-degrading protease release, may be related to plaque rupture [3–5]. In particular, immune cells of both innate and adaptive immunity may be activated by various endogenous molecules that have undergone chemical and/or structural modification following oxidative or glycation processes. In this way the immune system activation gives rise to low level inflammation leading to the slow development of atherosclerotic disease [6].
Intraplaque hemorrhage, a common event in vulnerable atherosclerotic lesions, results in the deposition of red blood cells (RBCs) and release of haemoglobin (Hb) [7]. The deposition of RBC membranes within atherosclerotic plaque, providing a large amount of lipids, represents a critical event in the plaque instability [8]. Several lines of evidence have led to attention to a possible pathogenic role of oxidized RBCs in atherogenesis, hypertension [9], coronary artery disease [10], and stroke [11, 12]. The crosstalk of RBCs with immune system has been investigated in the field of basic physiological processes [1, 2, 13–15]. We have recently provided evidence that oxidized RBCs present different immunomodulatory activities and suggested that these activities may contribute to perpetuation of inflammation in the pathogenesis of atherosclerosis [16, 17].
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Intraplaque hemorrhage, a common event in vulnerable atherosclerotic lesions, results in the deposition of red blood cells (RBCs) and release of haemoglobin (Hb) [7]. The deposition of RBC membranes within atherosclerotic plaque, providing a large amount of lipids, represents a critical event in the plaque instability [8]. Several lines of evidence have led to attention to a possible pathogenic role of oxidized RBCs in atherogenesis, hypertension [9], coronary artery disease [10], and stroke [11, 12]. The crosstalk of RBCs with immune system has been investigated in the field of basic physiological processes [1, 2, 13–15]. We have recently provided evidence that oxidized RBCs present different immunomodulatory activities and suggested that these activities may contribute to perpetuation of inflammation in the pathogenesis of atherosclerosis [16, 17].
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