Adalimumab Drug Suppresses Inflammation in Rheumatoid Arthritis Patients - European Medical Journal

Adalimumab Drug Suppresses Inflammation in Rheumatoid Arthritis Patients

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DISCOVERY of a new function in a widely used anti-inflammatory drug could offer new insight into the divergent efficacies of different medications which target the tumour necrosis factor (TNF).

Researchers from University College London, London, UK, have found that the monoclonal antibody adalimumab, commonly marketed under the brand name HUMIRA® (Abbvie Inc., North Chicago, Illinois, USA), does not only work by suppressing the target protein, TNF, as was previously assumed. Instead, adalimumab works by intensifying a particular function of the TNF protein when used to treat patients with rheumatoid arthritis (RA).

The antibody was found to enhance the ability of TNF, an inflammatory molecule produced by the immune system, to induce the formation of anti-inflammatory T cells. Adalimumab increases the expression of the TNF on the surface of patient monocytes and promotes the association of TNF molecules with the receptor proteins of T cells. This activates a signalling pathway giving the T cells the increased capacity to supress the inflammation.

Previous research conducted by the same authors found that treating RA with adalimumab increased the number of T cells. This was presumed to be the result of TNF blocking the development of these cells when adalimumab was absent. However, it is interesting to see that the use of etanercept, another TNF inhibitor, does not lead to the formation of these T cells supressing the inflammation resulting from RA.

This difference between the two is significant because it indicates potential diverging efficacies among TNF-targeting drugs to treat inflammatory diseases such as RA and Crohn’s disease. Furthermore, the discovery that adalimumab may both block the inflammatory responses of TNF and augment its activity towards resolving inflammation could offer new approaches of treatment. Prof Michael R. Ehrenstein, Consultant Rheumatologist, University College Hospital, London, UK, and study explained: “These results highlight how a treatment that targets a pivotal inflammatory cytokine not only preserves but actually boosts the pro-resolution forces driven by that pathway, thereby introducing a novel therapeutic paradigm.”


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