Why remission is not enough: underlying disease mechanisms in RA that prevent cure

For the past two decades, remission has been the focus of treatment strategies for rheumatoid arthritis (RA). This Review addresses the differences between remission and cure in RA and the underlying factors ('drivers') that trigger chronic inflammation and prevent cure. Cure is the aspirational aim for the treatment of all diseases, including chronic inflammatory conditions such as rheumatoid arthritis (RA); however, it has only been during the twenty-first century that remission, let alone cure, has been a regularly achievable target in RA. Little research has been carried out on how to cure RA, and the term 'cure' still requires definition for this disease. Even now, achieving a cure seems to be a rare occurrence among individuals with RA. Therefore, this Review is aimed at addressing the obstacles to the achievement of cure in RA. The differences between remission and cure in RA are first defined, followed by a discussion of the underlying factors (referred to as drivers) that prevent the achievement of cure in RA by triggering sustained immune activation and effector cytokine production. Such drivers include adaptive immune system activation, mesenchymal tissue priming and so-called 'remote' (non-immune and non-articular) factors. Strategies to target these drivers are also presented, with an emphasis on the development of strategies that could complement currently used cytokine inhibition and thereby improve the likelihood of curing RA.

Automated summary

This review article addresses the challenges and driving factors in achieving cure for rheumatoid arthritis (RA), highlighting the differences between remission and cure in RA. Strategies targeting these drivers are presented to improve the likelihood of curing RA, complementing current cytokine inhibition therapies.