IL-33 in autoimmunity; possible therapeutic target

Interleukin (IL)-33 is a member of the IL-1 cytokine family, which serves as both a cytokine and a nuclear factor. IL-33 is primarily expressed by keratinocytes, epithelial and endothelial cells, as well as human monocytes, Dendritic cells (DC), and astrocytes. IL-33 has been described as a modulator of inflammation and immune responses, which is mainly associated with the development of T helper 2 (Th2) immunological responses. Cytokines that control the T cells activation have been shown to have a role in the B-cell hyperactivity and production of pathogenic autoantibody isoforms that cause tissue dysfunction in autoimmune disorders. IL-33 levels have been shown to be elevated in a variety of autoimmune disorders, including Rheumatoid arthritis (RA), Systemic lupus erythematosus (SLE), type 1 diabetes (T1D), Multiple sclerosis (MS), and Inflammatory bowel diseases (IBD), suggesting that it may have a role in inducing autoimmunity and inflammatory damage. In addition to pathogenic functions in autoimmune disorders, cytokines may be a promising target for autoimmune disease treatment and follow-up. Therefore, the aim of this study is to review the possibility of using the IL-33/tumorigenicity 2 receptor (ST2) axis as a potential therapeutic target in the treatment of autoimmune disorders.