Significantly reduced function of T cells in patients with acute arterial thrombosis

To explore the intrinsic factors related to the pathogenesis of acute arterial thrombosis (AAT) and to elucidate the pathogenesis of AAT on the basis of differentially expressed genes.

Patients with acute myocardial infarction (AMI), stable angina (SA) and healthy controls (n = 20 per group) were recruited, and the whole human genome microarray analysis was performed to detect the differentially expressed genes among these subjects.

Patients with AMI had disease-specific gene expression pattern. Biological functional analysis showed the function of T cells was significantly reduced, the mitochondrial metabolism significantly decreased, the ion metabolism was abnormal, the cell apoptosis and inflammatory reaction increased, the phagocytosis elevated, the neutrophil-mediated immunity increased and the post-traumatic repair of cells and tissues increased in AMI patients. The biological function in SA group and healthy controls remained stable and was comparable.

The reduced function of T cell gene models in AAT showed the dysfunction of the immune system. The pathogenesis of AAT may be related to the inflammatory reaction after arterial intima infection caused by potential pathogenic microorganisms.