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Transfer of Manipulated Tumor-associated Neutrophils into Tumor-Bearing Mice to Study their Angiogenic Potential In Vivo
Published on: July 20, 2019
Tumor necrosis factor antagonist mechanisms of action: a comprehensive review
Daniel Tracey1, Lars Klareskog, Eric H Sasso
1Abbott Bioresearch Center, Worcester, MA, USA.
Abstract:
During the past 30 years, elucidation of the pathogenesis of rheumatoid arthritis, Crohn's disease, psoriasis, psoriatic arthritis and ankylosing spondylitis at the cellular and molecular levels has revealed that these diseases share common mechanisms and are more closely related than was previously recognized. Research on the complex biology of tumor necrosis factor (TNF) has uncovered many mechanisms and pathways by which TNF may be involved in the pathogenesis of these diseases. There are 3 TNF antagonists currently available: adalimumab, a fully human monoclonal antibody; etanercept, a soluble receptor construct; and infliximab, a chimeric monoclonal antibody. Two other TNF antagonists, certolizumab and golimumab, are in clinical development. The remarkable efficacy of TNF antagonists in these diseases places TNF in the center of our understanding of the pathogenesis of many immune-mediated inflammatory diseases. The purpose of this review is to discuss the biology of TNF and related family members in the context of the potential mechanisms of action of TNF antagonists in a variety of immune-mediated inflammatory diseases. Possible mechanistic differences between TNF antagonists are addressed with regard to their efficacy and safety profiles.
Insights
Tumor necrosis factor (TNF) plays a central role in immune-mediated inflammatory diseases like rheumatoid arthritis. TNF antagonists effectively treat these conditions, highlighting TNF
Area of Science:
- Immunology
- Molecular Biology
- Rheumatology
Background:
- Rheumatoid arthritis, Crohn's disease, psoriasis, psoriatic arthritis, and ankylosing spondylitis share common pathogenic mechanisms.
- Tumor necrosis factor (TNF) is implicated in the pathogenesis of these immune-mediated inflammatory diseases.
- Understanding TNF biology is crucial for developing targeted therapies.
Purpose of the Study:
- To review the biology of TNF and its family members.
- To discuss the mechanisms of action of TNF antagonists.
- To explore potential mechanistic differences between available TNF antagonists.
Main Methods:
- Review of scientific literature on TNF biology and immune-mediated inflammatory diseases.
- Analysis of the mechanisms of action of TNF antagonists (adalimumab, etanercept, infliximab).
- Comparison of efficacy and safety profiles of different TNF antagonists.
Main Results:
- TNF antagonists have demonstrated remarkable efficacy in treating immune-mediated inflammatory diseases.
- TNF is a central factor in the pathogenesis of these conditions.
- Differences in mechanisms of action may influence the efficacy and safety of TNF antagonists.
Conclusions:
- TNF antagonists are highly effective treatments for several immune-mediated inflammatory diseases.
- TNF antagonists represent a cornerstone in managing these conditions.
- Further research into mechanistic differences can optimize therapeutic strategies.
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