The opposite-direction modulation of CD4+CD25+ Tregs and T helper 1 cells in acute coronary syndromes

被引：115

作者：

Han, Shu-fang ^{[1
]}

Liu, Peng

Zhang, Wei

Bu, Lun

Shen, Min

Li, Hu

Fan, Yan-hong

Cheng, Kang

Cheng, He-xiang

Li, Cheng-xiang

Jia, Guo-liang

机构：

[1] Fourth Mil Med Univ, Xijing Hosp, Dept Cardiol, Xian 710032, Peoples R China

[2] Fourth Mil Med Univ, Dept Oral Histol & Pathol, Coll Stomatol, Xian 710032, Peoples R China

来源：

CLINICAL IMMUNOLOGY | 2007年 / 124卷 / 01期

关键词：

atherosclerosis; immunity; lymphocytes; destabilization;

D O I：

10.1016/j.clim.2007.03.546

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Different subsets of T lymphocytes have different functions in atherosclerosis advancement. T helper 1 cells and T regulatory 1 cells have been demonstrated to play opposite roles in rupture of atherosclerotic lesion. However, the role of novel subset of T regulatory cells, known as CD4+CD25+Foxp3+ T cells, remains largely unknown in coronary artery disease (CAD). In this study, we investigated the peripheral CD4+CD25+Foxp3+ T cells of patients with CAD and controls. The patients submitted were divided into three groups: stable angina pectoris (SA) group, unstable angina pectoris (UA) group and acute myocardial infarction (AMI) group. We analyzed the frequencies of peripheral CD4+CD25+Foxp3+ T cells and T helper 1/T helper 2 cells, expression of Foxp3 in CD4+CD25+ T subsets and cytokines pattern in patients and controls. We found that the reduction of CD4+CD25+Foxp3+ T lymphocytes was consistent with the expansion of Th1 cells in patients with unstable CAD. The reversed development between CD4+CD25+ Tregs and Th1 cells might contribute to plaque destabilization. (c) 2007 Elsevier Inc. All rights reserved.

引用

页码：90 / 97

页数：8

共 33 条

[21] Cutting edge:: Control of CD8+ T cell activation by CD4+CD25+ immunoregulatory cells [J].

Piccirillo, CA ;

Shevach, EM .

JOURNAL OF IMMUNOLOGY, 2001, 167 (03) :1137-1140

[22] Leukocyte-derived interleukin 10 is required for protection against atherosclerosis in low-density lipoprotein receptor knockout mice [J].

Potteaux, S ;

Esposito, B ;

van Oostrom, O ;

Brun, V ;

Ardouin, P ;

Groux, H ;

Tedgui, A ;

Mallat, Z .

ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2004, 24 (08) :1474-1478

[23] High donor FOXP3-positive regulatory T-cell (Treg) content is associated with a low risk of GVHD following HLA-matched allogeneic SCT [J].

Rezvani, Katayoun ;

Mielke, Stephan ;

Ahmadzadeh, Mojgan ;

Kilical, Yasemin ;

Savani, Bipin N. ;

Zeilah, Josette ;

Keyvanfar, Keyvan ;

Montero, Aldemar ;

Hensel, Nancy ;

Kurlander, Roger ;

Barrett, A. John .

BLOOD, 2006, 108 (04) :1291-1297

[24] Regulatory T cells: Key controllers of immunologic self-tolerance [J].

Sakaguchi, S .

CELL, 2000, 101 (05) :455-458

[25] T cell-mediated maintenance of natural self-tolerance: Its breakdown as a possible cause of various autoimmune diseases [J].

Sakaguchi, S ;

Toda, M ;

Asano, M ;

Itoh, M ;

Morse, SS ;

Sakaguchi, N .

JOURNAL OF AUTOIMMUNITY, 1996, 9 (02) :211-220

[26] Naturally arising CD4+ regulatory T cells for immunologic self-tolerance and negative control of immune responses [J].

Sakaguchi, S .

ANNUAL REVIEW OF IMMUNOLOGY, 2004, 22 :531-562

[27] Regulatory T cells in autoimmmunity [J].

Shevach, EM .

ANNUAL REVIEW OF IMMUNOLOGY, 2000, 18 :423-449

[28] Preference toward a T-helper type 1 response in patients with coronary spastic angina [J].

Soejima, H ;

Irie, A ;

Miyamoto, S ;

Kajiwara, I ;

Kojima, S ;

Hokamaki, J ;

Sakamoto, T ;

Tanaka, T ;

Yoshimura, M ;

Nishimura, Y ;

Ogawa, H .

CIRCULATION, 2003, 107 (17) :2196-2200

[29] Regulatory T cell responses develop in parallel to Th responses and control the magnitude and phenotype of the Th effector population [J].

Taylor, Justin J. ;

Mohrs, Markus ;

Pearce, Edward J. .

JOURNAL OF IMMUNOLOGY, 2006, 176 (10) :5839-5847

[30] Serum from patients with acute coronary syndromes displays a proapoptotic effect on human endothelial cells - A possible link to pan-coronary syndromes [J].

Valgimigli, M ;

Agnoletti, L ;

Curello, S ;

Comini, L ;

Francolini, G ;

Mastrorilli, F ;

Merli, E ;

Pirani, R ;

Guardigli, G ;

Grigolato, PG ;

Ferrari, R .

CIRCULATION, 2003, 107 (02) :264-270

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