Genetic deletion of Tfh cells and therefore, a reduction in GC B cells leads to attenuated atherosclerotic plaque burden in Apoe−/− as well as Ldlr−/− mice, whereas a promotion of GC formation via dysfunctional CD8+Tregs leads to accelerated atherosclerosis [151], indicating that GC-dependent IgGs play a proatherogenic role [56,152]. Here, LDLR is linked to atherosclerosis.