In LDLR−/− mice, abrogation of the invariant chain of CD74, a protein involved in MHCII-peptide complex formation [288], reduces T cell activation and atherosclerosis; however, in ApoE−/− mice, the inability to present antigens on MHCII increases atherosclerosis by reducing the pool of atheroprotective Tregs and increasing proatherogenic CD8+ T cells [289]. This evidence concerns the gene CD8A and atherosclerosis.