TY - JOUR
T1 - Functional T-lymphocyte dichotomy in the peripheral blood of patients with unstable angina
AU - Adler, Arnon
AU - Levy, Yair
AU - Roth, Arie
AU - Wexler, Dov
AU - Keren, Gad
AU - George, Jacob
PY - 2005
Y1 - 2005
N2 - OBJECTIVES. Herein, we investigated the percentage of T-helper (Th1) and Th2 cells among the general T-cell population in the peripheral blood of patients with stable angina (SA) and unstable angina (UA). BACKGROUND. Recent evidence suggests that Th1 cells and the cytokines that they secrete (especially IFN-γ) have a role in the activation of macrophages, promotion of clot formation and destabilization of atherosclerotic plaques. Thus, Th1 cytokines may contribute to the initiation and progression of UA. In contrast, cytokines secreted by Th2 cells (e.g. IL-10) are known to inhibit activation and proliferation of Th1 cells and the secretion of IFN-γ, lysosomal enzymes and metalloproteinases. Therefore, we sought to examine whether the ratio of IFN-γ to IL-10 secreting cells is altered in patients with UA. METHODS. The percentage of Th1 and Th2 cells among the general T-cell population was determined by fluorescent intracellular cytokine staining (IFN-γ and IL-10, out of the total CD3 positive cells). RESULTS. The percentage of T-cells positive for intracellular IFN-γ was significantly higher in patients with UA (n=22) in comparison with SA (n=20) patients (39.0 ± 2.8% and 29.6 ± 2.7%, respectively. P=0.02). There was no significant difference in intracellular IL-10 positive cells between the two groups. In addition, there was no significant difference in the ratio between the intracellular IFN-γ positive cells and the intracellular IL-10 positive cells. CONCLUSIONS. There is an increased activity of Th1 cells in patients with UA in comparison with patients with SA. There is no evidence of heightened activity of Th2 cells in either group. Thus, IFN-γ secreted by peripheral blood T-lymphocytes, may be an important immunomodulator contributing to destabilization of the atheromatous plaque lying at the base of the etiopathogenesis of unstable angina.
AB - OBJECTIVES. Herein, we investigated the percentage of T-helper (Th1) and Th2 cells among the general T-cell population in the peripheral blood of patients with stable angina (SA) and unstable angina (UA). BACKGROUND. Recent evidence suggests that Th1 cells and the cytokines that they secrete (especially IFN-γ) have a role in the activation of macrophages, promotion of clot formation and destabilization of atherosclerotic plaques. Thus, Th1 cytokines may contribute to the initiation and progression of UA. In contrast, cytokines secreted by Th2 cells (e.g. IL-10) are known to inhibit activation and proliferation of Th1 cells and the secretion of IFN-γ, lysosomal enzymes and metalloproteinases. Therefore, we sought to examine whether the ratio of IFN-γ to IL-10 secreting cells is altered in patients with UA. METHODS. The percentage of Th1 and Th2 cells among the general T-cell population was determined by fluorescent intracellular cytokine staining (IFN-γ and IL-10, out of the total CD3 positive cells). RESULTS. The percentage of T-cells positive for intracellular IFN-γ was significantly higher in patients with UA (n=22) in comparison with SA (n=20) patients (39.0 ± 2.8% and 29.6 ± 2.7%, respectively. P=0.02). There was no significant difference in intracellular IL-10 positive cells between the two groups. In addition, there was no significant difference in the ratio between the intracellular IFN-γ positive cells and the intracellular IL-10 positive cells. CONCLUSIONS. There is an increased activity of Th1 cells in patients with UA in comparison with patients with SA. There is no evidence of heightened activity of Th2 cells in either group. Thus, IFN-γ secreted by peripheral blood T-lymphocytes, may be an important immunomodulator contributing to destabilization of the atheromatous plaque lying at the base of the etiopathogenesis of unstable angina.
KW - Angina pectoris
KW - Atherosclerosis
KW - IFN-γ
KW - IL-10
KW - Lymphocytes
UR - http://www.scopus.com/inward/record.url?scp=27144457011&partnerID=8YFLogxK
U2 - 10.1080/14628840510039513
DO - 10.1080/14628840510039513
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AN - SCOPUS:27144457011
SN - 1462-8848
VL - 7
SP - 146
EP - 151
JO - International Journal of Cardiovascular Interventions
JF - International Journal of Cardiovascular Interventions
IS - 3
ER -