Abstract
Most inflammatory arthritides are systemic diseases. In an individual patient, however, disease flares are more common in joints affected previously, a phenomenon termed joint-specific memory. A key driver of localized recurrence is the accumulation of CD8+ T resident memory (T(RM)) cells in inflamed synovial tissues. These cells remain during remission and initiate recurrent disease when activated by arthritogenic antigens. The joint accumulation model is a paradigm that recognizes the contribution of local as well as systemic immune mechanisms to arthritis chronicity, highlighting new targets for disease intervention, including but not limited to T(RM) cells. The joint accumulation model underscores the importance of preventing extension of arthritis to new joints, even in established disease, translating into a rolling window of opportunity for optimal long-term arthritis management.