Background: gamma delta T cells are associated with the pathogenesis of coronary atherosclerotic heart disease, but the relationship between the development of acute myocardial infarction (AMI) and gamma delta T cells is not clear. So we attempt to investigate the expression pattern and clonality of T cell receptor (TCR) repertoire of gamma delta T cells in AMI patients, analyze the expression levels of regulatory genes Foxp3 and IL-17A, and characterize the correlation between gamma delta T cells and the pathogenesis of AMI. Methods: 25 patients diagnosed with ST-segment-elevation AMI were enrolled and 14 healthy individuals were recruited as the controls. RT-PCR and GeneScan were used to analyze the complementarity-determining region 3 sizes of TCR gamma delta repertoire genes in sorted gamma delta T cells from peripheral blood mononuclear cells (PBMCs). RQ-PCR was used to detect the gene expression levels of Foxp3, IL-17A and TCR V gamma subfamilies in sorted gamma delta T cells. All the patients were followed up for recordings of clinical endpoints. Results: The mRNA gene expression levels of TCR V gamma 1, V gamma 2, and V gamma 3 subfamilies in AMI patients were significantly higher than those in healthy controls. The expression pattern was V gamma 1 > V gamma 2 > V gamma 3 in AMI patients, while V gamma 1 > V gamma 3 > V gamma 2 in healthy controls. The significantly restricted expression of TCR Vd subfamilies were also found in AMI patients. The expression frequencies of TCR V delta 7 and TCR V delta 6 in AMI patients were significantly lower than those in healthy controls. The high clonal expansion frequencies of the TCR V delta 8, V delta 4 and V delta 3 were determined in AMI patients. High expression of Foxp3 gene was found in AMI PBMCs, while high expression of IL-17A was found in AMI gamma delta+ cells. Conclusions: Restrictive expression of TCR gamma delta repertoire and alteration expression of IL-17A gene are the important characteristics of gamma delta T cells in AMI patients, which might be related to the immune response and clinical outcome. gamma delta T cells might play a key role in the pathological progress of AMI and associated with the IL-17A mediated pathway.