LAUSR

The linkage of atherosclerosis to immune activation can be traced back as far as to Rudolf Virchow [1]. Cytokine release and alteration of surface marker expression on immune cells reflect this activation. Disorders characterized by a proinflammatory environment have been associated with an increased risk of atherosclerosis and many works implicate adaptive immunity in this risk [2, 3]. Advanced atherosclerotic plaques are enriched for activated T cells, thus pointing to their potential role in plaque progression and destabilization [4]. Nonetheless, the mechanisms of T-cell accumulation in plaques remain to be elucidated. To gain insight into these mechanisms, we analyzed the surface phenotypes of T cells isolated from human peripheral blood and autologous atherosclerotic plaques. Generally, immune cell phenotypes found in the plaques in our study are in agreement with those recently reported in mass cytometry (CyTOF) and singlecell RNA sequencing studies [5, 6]. Specifically, among plaque CD4+ and CD8+ T cells, the predominant population had a CD45RO+CD27effector memory phe-