Figure 2.

mTOR-inhibition affects atherosclerosis and myocardial infarction by modulation of immune cells. Stabilization of plaques is accomplished by less active CD8+ T cells and a shift of T helper cells to an antiinflammatory phenotype. Reduced chemoattraction reduces the number of monocytes/macrophages at the inflammation site, ameliorating inflammatory activity in both diseases. The shift of monocytes into a reparative phenotype limits the scar size. Even though enhanced antigen presentation in dendritic cells increases inflammatory activity, the shift toward tolerogenic DCs and stimulation of Treg function soothes inflammation and benefits the outcome after AMI. Reduced neutrophil activity lessens the collateral damage to viable myocardium in the border zone. B cell subpopulations exert contrary effects on atherosclerosis with yet unclarified outcome.