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It is conceivable that immunological processes driving disease remain active in patients even if clinical signs and disease symptoms are well-controlled through medication. A state of sustained, drug-free remission is rarely achieved. Rheumatoid Arthritis (RA), like most autoimmune diseases (AIDs), is a chronic inflammatory disease in which disease flares are common.

By doing so, we learn from their commonalities and differences. Hence, we learn from RA to build concepts and use our tools and knowledge to also study and translate them to other rheumatic AIDs, such as systemic sclerosis, ANCA-associated vasculitis and systemic lupus erythematosus. RA is a common and prototypic AID which has, in many ways, been at the forefront of discoveries of mechanistic insights that are applicable to AIDs on a broader scale. Therefore, with our team, we aim to delineate the molecular basis of (the absence of) immunological remission in RA. Insight into these phenomena is crucial to understand disease chronicity and for strategies aiming for permanent cure. To date, the nature of such ‘immunological disease activity’ is unclear, as are the strategies required to adress it and to reach immunological remission (rather than clinical remission).