Importantly, in patients and mouse models of SLE, interleukin-2 (IL-2) production is impaired, resulting in a decrease in regulatory T cells (Treg)—a subset of CD4+ T cells that maintain self-tolerance by suppressing autoreactive lymphocytes—as well as excessive differentiation of CD4+ naïve T cells into proinflammatory T helper 17 (Th17) cells or T follicular helper (Tfh) cells, causing inflammation and autoantibody production, respectively. This evidence concerns the gene IL2 and systemic lupus erythematosus.