Study Finds HUMIRA Doesn’t Just Inhibit TNF

Researchers from University College London have discovered that the anti-inflammatory drug HUMIRA doesn’t just work by inhibiting its target protein, TNF (tumor necrosis factor), but by enhancing a particular function of TNF in rheumatoid arthritis (RA) patients.

As indicated in the June 6, 2016 news release, “In prior research, Professor Michael Ehrenstein and colleagues at University College London found that treating RA patients with adalimumab increased the number of regulatory T cells capable of suppressing inflammation. Researchers presumed that this was because, in the absence of adalimumab, TNF blocks the development of these regulatory T cells. Mysteriously, however, another TNF inhibitor, etanercept, doesn’t induce the formation of these inflammation-suppressing T cells in rheumatoid arthritis patients.”

Professor Ehrenstein told OTW, “The unexpected result was that HUMIRA does not simply block the actions of TNF. In patients with rheumatoid arthritis it inhibits soluble TNF but boosts the actions of membrane TNF which activates regulatory T cells (the guardians of the immune system) thereby suppressing disease by an additional mechanism. Etanercept does not possess this regulatory T cell enhancing property.”