Studies have shown that IL-33 and ST2 were abnormally expressed in RA, SLE, SSc, and IBD, and the use of anti-ST2 antibodies reduced the production of IFN-γ, IL-17 and arthritis damage in mice, which indicated the potential role of IL-33 in AIDs (282). The gene discussed is IL17A; the disease is systemic lupus erythematosus.