Evidence for antigen-driven T-cell response in unstable angina

被引:94
作者
Caligiuri, G
Paulsson, G
Nicoletti, A
Maseri, A
Hansson, GK
机构
[1] Karolinska Inst, Ctr Mol Med, Stockholm, Sweden
[2] Hop Xavier Bichat, INSERM, U460, F-75018 Paris, France
[3] Hop Broussais, INSERM, U430, F-75674 Paris, France
[4] Catholic Univ, Cardiol Inst, Rome, Italy
关键词
angina; ischemia; prognosis; lymphocytes; antigens;
D O I
10.1161/01.CIR.102.10.1114
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background-Activation of T cells and macrophages has been associated with unstable angina (UA), but whether this reflects specific immune responses remains unclear. Methods and Results-We analyzed the repertoire and the length of complementarity -determining region 3 of the T cell receptor (TCR) beta-chain variable (BV) gene segments of activated lymphocytes in 23 patients with UA, 13 patients with chronic stable angina (CSA), and 6 normal control subjects. We also tested the proliferation of systemic T cells in response to autologous coronary plaque proteins, oxidized LDL, and Chlamydia pneumoniae as candidate antigens, in vitro. The activated T cell-TCRBV repertoire was perturbed in 13 (57%) of 23 UA patients versus 3 (23%) of 13 CSA patients (P=0.016) and was restricted to 6 (28%) of 21 expanded TCRBV families; all were significantly higher in UA than in CSA patients. At least one monotypic or oligotypic activated TCRBV population was found in 15 (65%) of 23 UA patients and in 3 (23%) of 13 CSA patients (P<0.001). Finally, T cells from UA patients, but not from CSA patients or normal control subjects, proliferated in response to autologous proteins from coronary culprit lesions and/or to oxidized LDL. Conclusions-Our findings suggest that the T-cell response observed in UA patients is antigen-driven and directed to antigens contained in the culprit coronary atherosclerotic plaques.
引用
收藏
页码:1114 / 1119
页数:6
相关论文
共 30 条
  • [1] Randomized secondary prevention trial of azithromycin in patients with coronary artery disease and serological evidence for Chlamydia pneumoniae infection -: The azithromycin in coronary artery disease:: Elimination of myocardial infection with Chlamydia (ACADEMIC) study
    Anderson, JL
    Muhlestein, JB
    Carlquist, J
    Allen, A
    Trehan, S
    Nielson, C
    Hall, S
    Brady, J
    Egger, M
    Horne, B
    Lim, T
    [J]. CIRCULATION, 1999, 99 (12) : 1540 - 1547
  • [2] Temporal relation between ischemic episodes and activation of the coagulation system in unstable angina
    Biasucci, LM
    Liuzzo, G
    Caligiuri, G
    Quaranta, G
    Andreotti, F
    Sperti, G
    vandeGreef, W
    Rebuzzi, AG
    Kluft, C
    Maseri, A
    [J]. CIRCULATION, 1996, 93 (12) : 2121 - 2127
  • [3] T-LYMPHOCYTE ACTIVATION IN STABLE ANGINA-PECTORIS AND AFTER PERCUTANEOUS TRANSLUMINAL CORONARY ANGIOPLASTY
    BLUM, A
    SCLAROVSKY, S
    SHOHAT, B
    [J]. CIRCULATION, 1995, 91 (01) : 20 - 22
  • [4] UNSTABLE ANGINA - A CLASSIFICATION
    BRAUNWALD, E
    [J]. CIRCULATION, 1989, 80 (02) : 410 - 414
  • [5] ROLE OF INFLAMMATION IN CORONARY PLAQUE DISRUPTION
    BUJA, LM
    WILLERSON, JT
    [J]. CIRCULATION, 1994, 89 (01) : 503 - 505
  • [6] Immune system activation follows inflammation in unstable angina: Pathogenetic implications
    Caligiuri, G
    Liuzzo, G
    Biasucci, LM
    Maseri, A
    [J]. JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1998, 32 (05) : 1295 - 1304
  • [7] Role of inflammation in the pathogenesis of unstable coronary artery disease
    Crea, F
    Biasucci, LM
    Buffon, A
    Liuzzo, G
    Monaco, C
    Caligiuri, G
    Kol, A
    Sperti, G
    Cianflone, D
    Maseri, A
    [J]. AMERICAN JOURNAL OF CARDIOLOGY, 1997, 80 : E10 - E16
  • [8] Gupta S, 1997, CIRCULATION, V96, P404
  • [9] Halme S, 1997, EUR HEART J, V18, P1095
  • [10] HANSSON GK, 1989, AM J PATHOL, V135, P169