Deciphering the mechanistic landscape of notch signaling in autoimmune pathogenesis

Autoimmune diseases are a group of disorders with multiple etiologies that disrupt normal immunological function, leading to the immune system mistakenly attacking the body’s own tissues. The Notch signaling pathway is a conserved pathway that is in part responsible for multiple cellular behaviors, including proliferation, differentiation, development, and death, through direct cell-to-cell communication. The expression and activation of Notch signaling pathway proteins are aberrantly regulated in autoimmune diseases in a manner that is closely related to their onset and development. We reviewed the functioning of the Notch signaling pathway in several autoimmune disorders, including rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), primary Sjögren’s syndrome (pSS), juvenile idiopathic arthritis (JIA), idiopathic thrombocytopenic purpura (ITP), multiple sclerosis (MS), autoimmune vasculitis, autoimmune hepatitis (AIH), autoimmune thyroid disease (AITD), autoimmune kidney diseases and type 1 diabetes mellitus (T1DM). We specifically sought to explore the involvement of the Notch signaling pathway in the occurrence and progression of RA to provide ideas and approaches for developing new therapeutic strategies for this autoimmune disease.