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) 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 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.
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