We investigate the contribution of circulating monocyte subsets as a source of a new isoform of tissue factor with angiogenic activity to the growth of intimal neovessel in atherosclerosis as a potential mechanism of lesion instability culminating in the onset of ischemic cardiovascular events (i.e. stroke and myocardial infarction).

We study the contribution of inflammatory cells infiltrating the atherosclerotic arterial wall to the progression of the disease:  identification of the cellular and molecular immune interactions that occur in the atherosclerotic plaque