Title:Cell Immunity in Coronary Artery Disease (CAD)
Volume: 11
Issue: 1
Author(s): Antonino Tuttolomondo, Irene Simonetta and Antonio Pinto
Affiliation:
Keywords:
Coronary Artery Disease (CAD), cell immunity, inflammation, lymphocytes.
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.