LDLR and atherosclerosis: We recently reported that atherosclerosis is increased in ApoE−/− mice upon inhibition of Treg recruitment in early atherosclerotic plaques by the genetic disruption of CCL1, while a similar effect is observed in LDLR−/− mice upon monoclonal antibody blockade of the CCL1-receptor CCR8, suggesting the importance of Treg recruitment in atherosclerosis development [404].