RIPK2 as a promising druggable target for autoimmune diseases

Receptor Interacting Serine/Threonine Kinase 2 (RIPK2) is an essential regulator of the inflammatory process and immune response. In innate immunity, the NOD-RIPK2 signaling axis is an important pathway that directly mediates inflammation and immune response. In adaptive immunity, RIPK2 may affect T cell proliferation, differentiation and cellular homeostasis thereby involving T cell-driven autoimmunity, but the exact mechanism remains unclear. Recent advances suggest a key role of RIPK2 in diverse autoimmune diseases (ADs) such as inflammatory bowel diseases, rheumatoid arthritis, multiple sclerosis, systemic lupus erythematosus, and Beh-cet's disease. This review aims to provide valuable therapeutic direction for ADs by focusing on the function and modulation of RIPK2 in innate and adaptive immunity, its involvement with various ADs and the application of RIPK2-related drugs in ADs. We raise the notion that drug targeting RIPK2 could be a promising therapeutic strategy for the treatment of ADs, though much work remains to be done for clinical application.

Automated summary

Receptor Interacting Serine/Threonine Kinase 2 (RIPK2) is a vital regulator in the inflammatory process and immune response. It plays a significant role in both innate and adaptive immunity, affecting inflammation, T cell proliferation, differentiation, and cellular homeostasis. Recent studies suggest the involvement of RIPK2 in various autoimmune diseases, making it a potential therapeutic target.