The therapeutic options for rheumatoid arthritis (RA) have increased immensely in the past two decades and resulted in improvements in outcome and quality of life. Especially, the arrival of biological and targeted synthetic disease-modifying anti-rheumatic drugs, with therapeutic targets ranging from cytokines (e.g. tumor necrosis factor to CD20 on B-cells, has dramatically improved the life of patients as exemplified by improved disease signs and symptoms together with less structural damage. However, these therapies have been proven not to be curative. Therefore, there is a clear need for a better understanding of the under- lying pathophysiology, including the contribution of the adaptive immune system and its window of opportunity for treatment in RA patients and individuals at risk of developing RA. Thus, the overarching aim of this thesis was to gain more knowledge on the adaptive immune response in different phases of RA and in various locations; ranging from the early at-risk phase to clinically apparent RA, from studies in blood-only to other bodily compartments, and from T-cells to B-cells
