OxLDL- and HSP-60 antigen-specific CD8+ T lymphocytes are detectable in the peripheral blood of patients suffering from coronary artery disease

被引:0
作者
M. Ghio
P. Fabbi
P. Contini
M. Fedele
C. Brunelli
F. Indiveri
A. Barsotti
机构
[1] University of Genoa,Department of Internal Medicine (DiMI) and Medical Specialties, I.R.C.C.S. “A.O.U. San Martino
[2] University of Genoa,IST”
来源
Clinical and Experimental Medicine | 2013年 / 13卷
关键词
OxLDL; HSP-60; Antigen-specific lymphocytes; Stable angina; Myocardial infarction;
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学科分类号
摘要
Inflammatory and immunologic mechanisms are important for the initiation and the progression of atherosclerotic lesions. OxLDL and HSP-60 antigens are involved in the pathogenesis of atherosclerotic disease by triggering immune cells within the plaques. Through the MHC pentamer assays, we investigated the presence of OxLDL- and HSP-60-specific CD8+ T lymphocytes in twenty HLA-A2-positive patients suffering from coronary artery disease (10 NSTEMI and 10 stable angina). Similarly, 10 age- and sex-matched healthy subjects were enrolled as controls. Biological samples were collected within 6 h of admission to hospital, at 30 days and at 180 days. OxLDL- and HSP-60-specific CD8+ T lymphocytes were never detectable in the peripheral blood from all the healthy controls. On the contrary, at each scheduled time point, both of these specific cells could be detected in peripheral blood from all enrolled patients. More in detail, the flow cytometric analysis of MHC-1 pentamer OxLDL-specific CD8+ T lymphocytes revealed a sharp and significant increase at the hospital admission, within 6 h from the chest pain onset, followed by an evident decline to lower levels at 30 days and at 180 days from the enrollment in the study. On the contrary, although MHC-1 pentamer HSP-60 CD8+ T lymphocytes were detectable in enrolled patients, almost no variance could be detectable during the follow-up scheduled evaluations. On the whole, this finding indicates that HSP-60- and OxLDL-specific CD8+ T lymphocytes could play a role in the maintenance or worsening of the atherosclerotic coronary disease.
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页码:251 / 255
页数:4
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