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1. Introduction
2. TNF: history
3. Why look for cytokines in rheumatoid arthritis?
4. The concept
5. Restimulation of autoantigen reactive T cells
6. Testing the concept: mediators
7. Many cytokines are produced in RS
8. Prolonged synthesis of IL-1-alpha in RS
9. Analysis of cytokine regulation
10. Cytokine cascade in rheumatoid arthritis
11. Cytokine cascade is physiological
12. Protection of joints in an animal model of RA
13. Rationale for anti-TNF-alpha therapy in RA
14. From bench to bedside
15. Remicade(R) (infliximab)
16. Open-label treatment with infliximab in RA
17. Randomised, placebo-controlled trial of infliximab
18. Evidence of efficacy of repeated infliximab therapy
19. Combination therapy - anti-TNF plus anti-CD4
20. Paulus 50% responses to infliximab
21. Rational of combination infliximab and MTX
22. Attract: sustained prevention of structural damage
23. Reversal of structural damage
24. Effectiveness of etanercept-MTX combination
25. Summary of anti-TNF therapy in RA
26. Antibody based therapeutic proteins
27. Adalimumab+MTX: sustained efficacy over 5 years
28. 7 years of etanercept therapy
29. Verifying mechanism of action in phase II useful
30. TNF-alpha dependent cytokine cascade in vivo
31. Other cytokines down regulated also
32. TNF is the body's fire alarm
33. TNF-alpha blockade and inflammatory cell traffic
34. Reduced PMN trafficking after infliximab therapy
35. Chronic inflamation diseases respond to anti-TNF
36. TNF is a good target in many chronic diseases
37. Reduced angiogenesis after anti-TNF
38. Cytokine washout with infliximab
39. Nothing is perfect: problems
40. Safety problems of TNF blockade
41. Early treatment is more effective
42. Prolonged reduction in disease activity
43. Impact on medicine and research
44. Impact on pharmaceutical industry
45. Acknowledgements (1)
46. Acknowledgements (2)
47. Acknowledgements (3)
48. Acknowledgements: funding

Topics Covered

• Immunological basis of rheumatoid arthritis (RA)
• Up-regulated cytokine expression is of major importance in RA
• Analysis of the disordered regulation shows that TNF blockade restored normal cytokine and destructive molecule levels and thus defined TNF as a therapeutic target
• Animal models of arthritis
• Clinical trials
• TNF has major input into leucocyte recruitment, it is thus the body's fire alarm
• TNF blockade and Crohn's disease, ulcerative colitis, ankylosing spondylitis, psoriasis, psoriatic arthritis and juvenile RA
• This represents the first major use for monoclonal antibodies in chronic diseases

Links

Series:

• Monoclonal Antibodies as Therapeutic Agents

Categories:

• Clinical Practice
• Immunology

Therapeutic Areas:

• Immunology & Inflammation

Talk Citation

Publication History

• Published on October 1, 2007
• Archived on June 13, 2019

Financial Disclosures

• Prof. Marc Feldmann has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.