Genetic inactivation of Cxcr3 or its ligand Cxcl10, that were both detected in mouse lesions in the ApoE−/− strain, resulted in decreased atherosclerosis burden that was accompanied by a decrease in inflammatory CD4+ T cell content, an elevated number of Tregs, and increased expression of IL-10 [78]. Here, CXCL10 is linked to atherosclerosis.