Recently, Meier et al. have shown that HD patients exhibited a reduction in the number of peripheral Tregs, which showed a reduced suppressor function. Considering the oxLDL effects, the relative percentage of Tregs of the total CD4 population was significantly reduced by incubation with oxLDL compared with a nonsignificant depleting effect on CD4+/CD25- T cells. The authors suggest that oxLDL have a specific role on Tregs. More interestingly, Tregs from HD patients exhibited early cell-cycle arrest and became apoptotic. These phenomena were the consequence of the oxLDL-inhibited proteasome proteolytic activity of p27Kip1 and Bax proteins, both of which accumulated in PHA-stimulated Tregs in vitro. Thus, plasma oxLDL in uremic patients might be the trigger of Tregs cycle arrest and apoptosis through proteasome alteration. Furthermore, they found that both uremic serum from HD patients and oxLDL triggered a time- and concentration-dependent down-regulatory effect on the expression of FOXP3. This means that circulating Tregs in HD patients, in addition to being reduced in number, also expressed low levels of FOXP3 per cell, and thus failed to suppress the proliferation of effector cells.