The outlook for patients with rheumatoid arthritis (RA) has brightened significantly in recent years. Improvements in imaging enable both disease detection at a very early stage and the assessment of even minor disease progression.
Potential biomarkers hold promise for refined diagnosis, treatment selection and monitoring. The range of available treatments for people living with RA has expanded markedly thanks to our increasing understanding of disease pathophysiology. However, despite these advances, significant unmet need remains: a substantial proportion of patients still do not achieve sustained remission, today’s recognised treatment goal.
RA is a highly complex inflammatory disease
The pathogenesis of RA is driven by a complex interaction of pro-and anti-inflammatory pathways involving many cellular and molecular mediators. The consequence is sustained inflammation in the soft inner lining of articular joints – the synovial tissue. This causes severe pain, swelling and stiffness, and can lead to permanent damage and deformity in structural joint elements like cartilage and bone. Some organ systems – such as cardiac tissue, the vascular system, kidneys, lung tissue and the nervous system – may ultimately also be damaged by systemic inflammation.
Autoantibodies – potentially harmful, pathogenic antibodies that can produce an abnormal response from the body’s immune system in which it conducts a sustained attack on a person’s own cells, tissues and organs – have been implicated in chronic conditions, including RA. In RA, autoantibodies are highly prevalent and may significantly contribute to the development and progression of this chronic inflammatory disease. Selectively blocking these autoantibodies may hold a key to alleviating disease for many patients who lack or lose response to current therapies.
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