Based on the results to our study and current literature, we speculate that in healthy vessels, there is basal level of T cell infiltration that may be required for immune surveillance. During hypertension, there is greater T cell infiltration localized to the perivascular fat of the aorta. Although each T cell infiltrate produces that same amount of cytokines as in healthy vessels, greater T cell infiltrate during hypertension may result in an overall net increase cytokines produced. However, indicative of a phenotypical difference, T cell infiltrates in vessels of hypertensive mice produce greater CCL2 and ROS, which can result in enhanced leukocyte recruitment such as macrophages (MΦ), oxidative stress and local inflammation that can lead to vascular dysfunction and exacerbate hypertension.