Cytokine therpay



by Nathan Wei, MD, FACP, FACR

Nathan Wei is a nationally known board-certified rheumatologist and author of the Second Opinion Arthritis Treatment Kit. It's available exclusively at this website... not available in stores.

Click here: Second Opinion Arthritis Treatment Kit


The role of cytokines in rheumatoid arthritis is the subject of interest in the field of rheumatology. The first biologic drugs shown to have a profound effect in rheumatoid arthritis were the anti-TNF drugs. These drugs blocked the effects of the pro-inflammatory cytokine, tumor necrosis factor-alpha.

Here are excerpts from an excellent review that appeared in Arthritis Treatment and Research.

Anti-cytokine therapy in chronic destructive arthritis

Wim B van den Berg

Department of Rheumatology, University Medical Center St Radboud, Nijmegen, The Netherlands

Arthritis Res 2001, 3:18-26 doi:10.1186/ar136

© 2000 BioMed Central Ltd on behalf of the copyright holders



"The synovial reaction in RA patients is characterized by the abundance of many cytokines, chemokines and growth factors. It is now generally accepted that TNF and IL-1 are master cytokines in the process of chronic joint inflammation and the concomitant erosive changes in cartilage and bone. Proinflammatory and destructive properties were first demonstrated in culture studies in vitro and the arthritogenic potential of TNF and IL-1 was substantiated by arthritis induction in rodents.

Both animal model studies and clinical observations have contributed greatly to the identification of TNF and IL-1 as useful therapeutic targets. Apart from the obvious demonstration that arthritis in TNF transgenic mice could be blocked with anti-TNF antibodies, it was a major breakthrough to note that collagen type II arthritis, the classical RA model in rodents, could be suppressed with anti-TNF antibodies or TNF soluble receptors.

In addition to the evidence from studies on animal models, the cytokines TNF and IL-1 were demonstrated in increased quantities in RA synovial tissue, along with the presence of cell-associated receptors for these cytokines… The remarkable anti-inflammatory activity of a first neutralizing monoclonal anti-TNF antibody in RA patients revealed the potential of anti-cytokine therapy… and has subsequently stimulated the development of improved anti-TNF reagents such as fully humanized antibody and engineered fusion proteins of TNF soluble receptors and Fc fragments, with reduced immunogenicity and a prolonged half-life. There is no doubt that TNF blockers provide impressive protection against pain and joint swelling in most RA patients…. It is also evident that anti-TNF therapy is not effective in all RA patients, nor does it control arthritis in all affected joints of good responders.

Remarkably, the recent evaluation of joint erosions after the treatment of RA patients with anti-TNF provided the first evidence for a joint protective effect, as reported at the 1999 ACR meeting. This was shown for a combination of anti-TNF antibodies with methotrexate, and also for a single treatment with antibodies as well as TNF soluble receptor. Unfortunately, the actual data have not yet been published, hampering detailed attention in this review. The finding might fit with the hypothesis that TNF overproduction in RA synovial tissue is mainly caused by deranged behaviour of synoviocytes, generating too much TNF. If this is so, TNF will drive IL-1 production and TNF blockade will be sufficient to control this TNF–IL-1 pathway. Anti-TNF antibodies used in clinical studies display cytotoxic effects."

In addition to anti-TNF as a cytokine inhibitor, there have been others that have also been shown to be effective. A prime example is tocilizumab (Actemra) which inhbits interleukin-6, a potent pro-inflammatory cytokine.



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