Peripheral T cell receptor beta immune repertoire is promptly reconstituted after acute myocardial infarction.

ABSTRACT

BACKGROUND: Acute myocardial infarction (AMI) is characterized by an inflammatory process in which T cell plays a key role. However, the profile of immune microenvironment in AMI is still uncertain. High-throughput sequencing of T cell receptor (TCR) provides deep insight into monitoring the immune microenvironment. METHODS: 30 patients with AMI were enrolled and 30 healthy individuals were recruited as controls. Flow cytometer were used to analyze the distribution of αß T cells and their CD69 expression from peripheral leukomonocytes. TCRß repertoire library was amplified by two-round multiplex PCR and detected by next-generation sequencing (NGS). RESULTS: The percentage of αß T cells in AMI patients were significantly restricted than those in healthy controls, while the highly activated αß T cells along with distinguishing usage of variable (V), diversity (D) and joining (J) gene segments were also found in AMI patients. In addition, AMI induced a significantly restricted CDR3 amino acid (AA) diversity and remarkably reconstituted TCR immune repertoires. Finally, we identified several AMI-associated tendency of CDR3 AAs expression after AMI. CONCLUSIONS: Our work suggests that the aberrant αß T cells distribution and activation may associated with the pathogenesis of AMI and demonstrates a reconstitution of TCRß immune repertoire after AMI.