In the (NZB × NZW) F1 mouse model of lupus and in human SLE patients we found that an acquired deficiency of IL-2 caused a homeostatic disbalance between proliferating Treg and conventional CD4+ T cells (Tcon), which was accompanied by the loss of CD25 expression on Treg and an accelerated Tcon hyperactivity in lymphatic organs and peripheral blood [14,15]. Here, IL2 is linked to systemic lupus erythematosus.