Mechanisms and Clinical Applications of Infliximab in Rheumatoid Arthritis and Crohn's Disease Management
Received Date: Jun 01, 2024 / Published Date: Jun 29, 2024
Abstract
Infliximab, a monoclonal antibody targeting tumor necrosis factor alpha (TNF-alpha), has revolutionized the management of chronic inflammatory diseases such as rheumatoid arthritis (RA) and Crohn's disease (CD). This review explores the intricate mechanisms through which Infliximab exerts its therapeutic effects and its clinical applications in the treatment of RA and CD. The primary mechanism of action involves the binding of Infliximab to soluble and transmembrane TNF-alpha, thereby neutralizing its pro-inflammatory effects. By inhibiting TNF-alpha, Infliximab mitigates inflammation, reduces joint destruction in RA, and alleviates intestinal inflammation in CD. This dual action underscores its efficacy in suppressing disease activity and improving patient outcomes. Clinical studies have demonstrated the efficacy of Infliximab in achieving sustained remission and improving quality of life for patients with RA and CD refractory to conventional therapies. However, challenges such as the development of anti-drug antibodies and infusion reactions necessitate careful monitoring and management strategies. Moreover, advancements in personalized medicine have enabled the optimization of Infliximab therapy through biomarkerguided dosing and the identification of predictors of treatment response. Future directions include the exploration of combination therapies and novel formulations to enhance efficacy and reduce immunogenicity. In conclusion, Infliximab stands as a cornerstone in the therapeutic armamentarium for RA and CD, offering profound relief and disease control for patients. Continued research efforts are crucial to unraveling its full potential and ensuring its optimal utilization in clinical practice.
Citation: Wilson K (2024) Mechanisms and Clinical Applications of Infliximab inRheumatoid Arthritis and Crohn's Disease Management. J Pulm Res Dis 8: 205.
Copyright: © 2024 Wilson K. This is an open-access article distributed under theterms of the Creative Commons Attribution License, which permits unrestricteduse, distribution, and reproduction in any medium, provided the original author andsource are credited.
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