Adalimumab Inhibits the Bad, Enhances the Good

A new study conducted by researchers from University College London has documented a new mechanism of action for adalimumab, the anti-inflammatory medication that is widely prescribed for patients with rheumatoid arthritis. In addition to inhibiting its target protein, TNF, the study concludes that adalimumab, marketed as HUMIRA®, promotes membrane TNF-TNF-RII binding thereby enhancing the production of anti-inflammatory T cells. The findings were published online this week in Journal of Experimental Medicine.

TNF inhibitors are widely used to treat inflammatory diseases that include Crohn’s disease as well as rheumatoid arthritis. It had been preciously observed that patients treated with adalimumab showed increased presence of T cells capable of suppressing inflammation, but the effect was presumed to stem from the inhibition of TNF that blocks the development of these cells. Instead, this study found that adalimumab both blocks the proinflammatory functions of soluble TNF and augments the activity of membrane-bound TNF that combats inflammation. Michael Ehrenstein, PhD, Consultant Rheumatologist at UCL Hospitals and co-author of the study, commented, “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.”

Read a Pain Reporter interview with Dr. Ehrenstein, here.

Read more about Humira or rheumatoid arthritis.

Read a news report about the discovery, with link to the journal article, here.

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