Abstract
Objective: Both adaptive and innate immune systems are involved in coronary artery disease (CAD). The aim of this study was to evaluate TH17 cytokines expression profiles in un-stimulated peripheral blood lymphocytes (PBMCs) of patients with coronary artery disease. Methods: Expression profiles of IL-17, IL-23, and TGF-β1 were determined in individuals with and without CAD using Real-time PCR. Results: A significant decrease in IL-23 gene expression in un-stimulated PBMCs of patients with CAD compared to those without CAD was found (p=0.003, OR=0.045, 95% CI: 0.006–0.355). Conclusion: Our data reinforce the potential role of the IL-23 as a critical regulatory molecule that bridges the innate and adaptive arms of the immune system in the complex mechanisms associated with the development of atherosclerosis.
Highlights
Atherosclerosis is a chronic inflammatory disease of vessel walls with involvement of both innate and adaptive immune system [1]
Several lines of evidence driven from numerous functional genomic studies support the fact that immune cells especially T cells play a critical role during lesion development in atherosclerosis [10]
We have found a significant down-regulation of IL-23 gene expression in un-stimulated peripheral blood lymphocytes (PBMCs) of patients with coronary artery disease (CAD)
Summary
Atherosclerosis is a chronic inflammatory disease of vessel walls with involvement of both innate and adaptive immune system [1]. Several lines of evidence based on animal models and humans studies suggest that immune cells directly participate in development of the atherosclerotic plaques [1,2]. Considerable evidence supports the involvement of adaptive immune system in development and progression of coronary artery disease (CAD) [3]. The role of Th2 pathway in atherosclerotic process is still controversial depending on the experimental model studied and the stage and/or site of the lesion. Th-17 and Treg cells have emerged as important regulators of inflammatory reactions in CAD. The contribution of these cell types as possible participants in atherosclerotic lesion development is indicating the complex mechanisms and the variety of cell types involved in disease process [6,7,8]
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