The role of TNF - α signaling pathway in rheumatoid arthritis and the therapeutic progress of TNF-α monoclonal antibodies

Abstract

Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic synovitis and progressive joint destruction. Tumor necrosis factor - α (TNF - α) plays a central regulatory role in its inflammatory network. At present, biological agents such as TNF - α monoclonal antibodies (mAbs) have been widely used in clinical practice, significantly improving the prognosis of RA patients. But some patients have problems with poor treatment efficacy or infection. The differences and safety issues between different drugs still need further research. This article analyzes the immune imbalance mechanism of RA and the activation process of TNF - α signaling pathway, explores the mechanism of action and safety characteristics of TNF - α inhibitor drugs (adalimumab, infliximab, etanercept), and reviews the research progress of new inhibitors such as biosimilars. TNF - α inhibitors can effectively block downstream inflammatory signals and alleviate joint damage. However, there are significant differences in patients' response to treatment, and issues related to infection risk and immunogenicity limit the long-term use of drugs. This study provides a theoretical reference for investigating the mechanism of TNF - α targeted therapy for rheumatoid arthritis. At the same time, future research should focus on exploring biomarkers for predicting treatment response, optimizing individualized combination therapy, and developing new drugs for nontumor necrosis factor pathways to cover a wider range of patients.