Recent studies showed that mice deficient in IL-2 or IL-2 receptor components, including CD25 and CD122, succumb to a rapidly progressing autoimmune disease characterized by uncontrolled activation of T and B cells and by generating autoantibodies (Suzuki et al. 1995), which was consistent with typical immunological features of SLE. This evidence concerns the gene IL2 and systemic lupus erythematosus.