SLE is a chronic autoimmune connective tissue disease that develops mainly due to an imbalance between pro-inflammatory factors (e.g., IFN-g, TH17) and regulatory cytokines (e.g., IL-2) (Gatto et al., 2013), leading to the production of multiple antibodies, the formation and deposition of immune complexes, and the interaction between the two leading to organ and tissue damage (Leng et al., 2010), resulting in clinical manifestations such as fever, headache, rash, and kidney damage. Here, IL2 is linked to systemic lupus erythematosus.