Furthermore, in line with similar data from diabetic NOD mice [56], a recent report demonstrates that lupus pathogenesis in NZB/W F1 mice could be either accelerated by IL-2 neutralization or impeded by IL-2 complementation [18], and proposes a pathogenesis model driven by interdependent Treg and IL-2 deficiencies. Here, IL2 is linked to systemic lupus erythematosus.