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Cell Journal، جلد ۱۳، شماره Supplement، صفحات ۰-۰
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عنوان انگلیسی P-11: Considering CD4+Foxp3+Treg Cellsand ICOS+ Molecule Expression in Patient with Myocardial Infraction
چکیده انگلیسی مقاله Objective: Atherosclerosis is a multifactorial disorder that immune mechanisms play an important role in its pathogenesis. Naturally occurring CD4+Foxp3+ regulatory T cells (Tregs) exert suppressive effects on effector CD4 cells and regulate immunological response. ICOS molecule expression by Treg has been reported to identify a Treg subtype with high suppressive potential (ICOS + Treg). We have hypothesized that Peripheral CD4 + Foxp3 + Treg number reduction and shift toward ICOS-population would be account for plaque progression and instability. We investigated here the frequency of circulating CD4 + Foxp3 + Treg and it's ICOS+subset in patient with myocardial infraction (MI) in comparison with stable angina (SA) patients as well as normal coronary angiography subjects. Materials and Methods: Peripheral blood mononuclear cells were isolated by Ficol solution from 25 normal coronary angiography subjects (control) , 27 SA patients and 28 MI Patients. Peripheral numbers of Treg were evaluated by FACS employing labeled antibodies to CD4 and Foxp3 and ICOS. Comparison among the groups was carried out employing the one-way ANOVA Results: We found significantly lower Treg cells frequency in patients with coronary heart disease (MI and SA) as compared with controls (1.93 ± 1%, 2.94 ± 1.18% Vs. 4.09 ± 1.16% respectively p< 0.001). Treg cells frequencies markedly decreased in patients with MI compared to patients with SA (p=0.005). In addition there was observed that ICOS + /ICOS- ratio was shifted toward the ICOS- population in atherosclerosis patients (MI: 1.06 ± 0.6, SA: 1.24 ± 0.46, Control: 1.63 ± 0.65, p=0.002). Conclusion: Our data suggest that Treg cells have a potentially protective role in atheroma progression and stability. It seems enhancement of Treg responses, through manipulation of the ICOS pathway, has potential as a therapeutic strategy for atherosclerotic disease
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نشانی اینترنتی http://celljournal.org/journal/article/abstract/1543
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