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Differential expression of T cell-related genes in AMI and SA stages of coronary artery disease.
OBJECTIVE: To identify differentially expressed T cells-related genes in peripheral blood mononuclear cells and compare their differences in T cell activation and subset functions in different stages of coronary atherosclerosis disease (CAD).
METHODS: 20 patients with acute myocardial infarction patients (AMI), 20 patients with stable angina pectoris (SA) and 20 healthy volunteers were recruited into the study. Whole human genome microarray analysis was used to detect the expression of T cell related genes among three groups.
RESULTS: mRNA expression of 68 genes involved in T cell was detected. 1) Antigen recognition: in the AMI patients 12 genes were down-regulated and 9 were significantly down-regulated among all 13 genes, compared with those of the SA and the control group, respectively. 2) Co-stimulators and regulators of T cell activation: among 16 genes in the AMI patients, 15 genes were lower and 8 were significantly lower than the other two groups. 3) T cell subsets, CTL: all 11 genes in the AMI patients were down-regulated, particularly GZMM and CASP8 were significantly down-regulated compared with the SA patients and controls. Th1/Th2: in the AMI patients, gene expressions including IL1 and IL18 were significantly higher, whereas GATA3 mRNA was significantly lower than those in other two groups. Th17/Treg: in the AMI group, RORC and CCR6 mRNAs were significantly down-regulated compared with the control group, while CD25 and CD127 expressions were significantly lower than SA group. There was no difference in T cell related genes between the SA patients and the controls.
CONCLUSIONS: In the AMI patients, the mRNA expression of T cell antigen recognition, activation and subset functions was imbalanced or decreased, indicating the dysfunction of cellular immunity in patients with AMI. Then improving T cell mediated cellular immunity may be considered as a potential target for medical interventions in the patients with AMI.
METHODS: 20 patients with acute myocardial infarction patients (AMI), 20 patients with stable angina pectoris (SA) and 20 healthy volunteers were recruited into the study. Whole human genome microarray analysis was used to detect the expression of T cell related genes among three groups.
RESULTS: mRNA expression of 68 genes involved in T cell was detected. 1) Antigen recognition: in the AMI patients 12 genes were down-regulated and 9 were significantly down-regulated among all 13 genes, compared with those of the SA and the control group, respectively. 2) Co-stimulators and regulators of T cell activation: among 16 genes in the AMI patients, 15 genes were lower and 8 were significantly lower than the other two groups. 3) T cell subsets, CTL: all 11 genes in the AMI patients were down-regulated, particularly GZMM and CASP8 were significantly down-regulated compared with the SA patients and controls. Th1/Th2: in the AMI patients, gene expressions including IL1 and IL18 were significantly higher, whereas GATA3 mRNA was significantly lower than those in other two groups. Th17/Treg: in the AMI group, RORC and CCR6 mRNAs were significantly down-regulated compared with the control group, while CD25 and CD127 expressions were significantly lower than SA group. There was no difference in T cell related genes between the SA patients and the controls.
CONCLUSIONS: In the AMI patients, the mRNA expression of T cell antigen recognition, activation and subset functions was imbalanced or decreased, indicating the dysfunction of cellular immunity in patients with AMI. Then improving T cell mediated cellular immunity may be considered as a potential target for medical interventions in the patients with AMI.
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