B6-Yaa mutant mice developed systemic lupus erythematous-like disease in association with a defect in CD8+CD122+ Treg activity, suggesting that the Treg subset may be utilized to treat systemic lupus erythematous-like autoimmune disease.[15] Therefore, in multiple experimental animal models, CD8+CD122+ Tregs play an important role in the suppression of various autoimmune diseases. This evidence concerns the gene IL2RB and autoimmune disease.