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CD4⁺Foxp3⁺ Treg and its ICOS⁺ Subsets in Patients with Myocardial Infarction | ||
Iranian Journal of Immunology | ||
مقاله 5، دوره 9، شماره 1، خرداد 2012، صفحه 53-60 اصل مقاله (447.28 K) | ||
نوع مقاله: Original Article | ||
نویسندگان | ||
Samira Ghorbani Gazar1؛ Alireza Andalib* 1؛ Mohammad Hashemi2؛ Abbas Rezaei1 | ||
1Department of Immunology | ||
2Department of Internal Medicine, Isfahan Medical School, Isfahan University of Medical Sciences, Isfahan, Iran | ||
چکیده | ||
Background: Atherosclerosis is a multifactorial disorder with chronic inflammatory conditions in which immune cells play a significant role in its pathogenic process. Regulatory T cells (Treg), as a part of immune system, are involved in controlling autoimmune and inflammatory diseases. Quantitative and/or functional alteration of Tregs has been shown to play an atheroprotective role and may also promote plaque stabilization. Objective: To assess if inducible costimulatory molecule (ICOS) expression on one subtype of Treg cells with high suppressive potential correlates with the pathogenesis of atherosclerosis. Methods: Patients with myocardial infarction (MI) and/or stable angina (SA), diagnosed as atherosclerosis by angiography, and a group of individuals with normal coronary angiography (NCA) were recruited for the present study. Peripheral blood mononuclear cells (PBMCs) were prepared and the expression of ICOS, Foxp3 and CD4 molecules was tested by flowcytometry. Results: The percentage of CD4+Foxp3+ Treg cells was reduced in MI group compared to NCA and SA groups (p<0.005). Evaluation of the two Treg subsets according to ICOS expression showed a decreased ICOS+/ICOS- Treg ratio in MI and SA groups compared to NCA individuals (p=0.002 and p=0.048, respectively). Conclusion: The present data indicate that Tregs and its ICOS+ subsets are decreased in patients with MI or SA, suggesting a potential role for Treg in atherosclerosis progression or onset of acute coronary syndrome. | ||
کلیدواژهها | ||
Acute coronary syndrome؛ Atherosclerosis؛ ICOS؛ myocardial infarction؛ Regulatory T cells؛ Stable Angina | ||
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