Abstract
Numerous researches have detected immune cellular elements in coronary lesions of atherosclerotic origin in human and animal models, and these cells are suspected of contributing to plaque instability. Patients affected by acute coronary syndrome present high levels of pro-inflammatory molecules, as shown in numerous studies. This finding implies similarity between CAD and well-known immune-mediated inflammatory diseases. Due to incongruent findings, this “infection hypothesis” cannot be rejected, thus further research is needed to better understand the relationship between pathogen-induced chronic inflammatory response, with its pathogenic mechanisms, and the atherosclerotic process. Several clinical studies have consistently reported the involvement of polymorphonuclear neutrophils in atherosclerotic coronary disease; autoptic studies have showed their presence in unstable lesions. The evidence of their features of activation suggests that polymorphonucleates take part in atherosclerotic pathogenesis and in its worst evolution. The evidence of a systemic activation of T lymphocytes in individuals affected by ischemic heart disease, as shown in recent work, underlines the significant role of adaptive immunity in this pathological condition. Three subpopulations of T-cells with unusual features have been described: CD4+CD28- T lymphocytes, which lack of CD28 expression (CD28 is a co-stimulatory molecule engaged in the antigen recognition by T lymphocytes), naturally occurring regulatory T-lymphocytes and interleukin-17-producing T-cells. To date the main therapeutic target is coronary thrombosis, which represents the final event causing life threatening complications related to atherosclerosis, so targeting immune cells could represent a future therapeutic aim.
Keywords: Coronary Artery Disease (CAD), cell immunity, inflammation, lymphocytes.
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