TY - JOUR
T1 - Increased expression of T cell activation markers (CD25, CD26, CD40L and CD69) in atherectomy specimens of patients with unstable angina and acute myocardial infarction
AU - Hosono, Mitsuharu
AU - de Boer, Onno J.
AU - van der Wal, Allard C.
AU - van der Loos, Chris M.
AU - Teeling, Peter
AU - Piek, Jan J.
AU - Ueda, Makiko
AU - Becker, Anton E.
PY - 2003
Y1 - 2003
N2 - Atherosclerotic plaques contain a chronic immune mediated inflammation in which T cells play an important role. A previous study revealed that the numbers of interleukin-2 receptor-positive T cells is increased in culprit lesions of patients with acute coronary syndromes; a finding of considerable interest since it indicates a recent change in the intraplaque T cell mediated immune response. Confirmation of this observation is important, because it could provide insight into the onset of the acute event. We have, therefore, expanded our earlier work by using a panel of different T cell activation markers (CD25, CD26, CD40L, CD69). The study is based on 58 culprit lesions from patients who underwent coronary atherectomy. There were four groups of patients: chronic stable angina (n = 13), stabilized unstable angina (n = 16), refractory unstable angina (n = 15), and acute myocardial infarction (AMI; n = 14). Activated T cells were expressed as a percentage of the total of CD3-positive cells. CD25, CD26, CD40L, and CD69/CD3 percentages increased with the severity of the coronary syndrome. In patients with AMI all percentages were significantly higher than in patients with chronic stable angina. CD25, CD26, CD40L, and CD69/CD3 percentages in patients with an unstable condition (refractory unstable angina and AMI) were significantly higher than those in patients with a stable condition (chronic stable or stabilized unstable angina) The finding that the percentage of T cells with recent onset activation is significantly increased in the culprit lesions of patients with acute coronary syndromes suggests strongly that a recent change in pathogenic stimulation has occurred leading to local T cell activation. (C) 2003 Elsevier Science Ireland Ltd. All rights reserved
AB - Atherosclerotic plaques contain a chronic immune mediated inflammation in which T cells play an important role. A previous study revealed that the numbers of interleukin-2 receptor-positive T cells is increased in culprit lesions of patients with acute coronary syndromes; a finding of considerable interest since it indicates a recent change in the intraplaque T cell mediated immune response. Confirmation of this observation is important, because it could provide insight into the onset of the acute event. We have, therefore, expanded our earlier work by using a panel of different T cell activation markers (CD25, CD26, CD40L, CD69). The study is based on 58 culprit lesions from patients who underwent coronary atherectomy. There were four groups of patients: chronic stable angina (n = 13), stabilized unstable angina (n = 16), refractory unstable angina (n = 15), and acute myocardial infarction (AMI; n = 14). Activated T cells were expressed as a percentage of the total of CD3-positive cells. CD25, CD26, CD40L, and CD69/CD3 percentages increased with the severity of the coronary syndrome. In patients with AMI all percentages were significantly higher than in patients with chronic stable angina. CD25, CD26, CD40L, and CD69/CD3 percentages in patients with an unstable condition (refractory unstable angina and AMI) were significantly higher than those in patients with a stable condition (chronic stable or stabilized unstable angina) The finding that the percentage of T cells with recent onset activation is significantly increased in the culprit lesions of patients with acute coronary syndromes suggests strongly that a recent change in pathogenic stimulation has occurred leading to local T cell activation. (C) 2003 Elsevier Science Ireland Ltd. All rights reserved
U2 - https://doi.org/10.1016/S0021-9150(03)00024-8
DO - https://doi.org/10.1016/S0021-9150(03)00024-8
M3 - Article
C2 - 12732389
SN - 0021-9150
VL - 168
SP - 73
EP - 80
JO - Atherosclerosis
JF - Atherosclerosis
IS - 1
ER -