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Abstract
Pain is one of the most debilitating symptoms of rheumatoid arthritis (RA), and yet remains poorly understood, especially when pain occurs in the absence of synovitis. Without active inflammation, experts most often attribute joint pain to central nervous system dysfunction. However, advances in the past 5 years in both immunology and neuroscience research suggest that chronic pain in RA is also driven by a variety of abnormal interactions between peripheral neurons and mediators produced by resident cells in the local joint environment. In this Review, we discuss these novel insights from an interdisciplinary neuro-immune perspective. We outline a potential working model for the peripheral drivers of pain in RA, which includes autoantibodies, resident immune and mesenchymal cells and their interactions with different subtypes of peripheral sensory neurons. We also offer suggestions for how future collaborative research could be designed to accelerate analgesic drug development.
Original language | English |
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Pages (from-to) | 671-682 |
Number of pages | 12 |
Journal | Nature Reviews Rheumatology |
Volume | 20 |
Issue number | 11 |
Early online date | 6 Sept 2024 |
DOIs | |
Publication status | Published - Nov 2024 |
Keywords
- pain, rheumatoid arthritis, neuro-immune
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WTCA: Fibroblasts as key drivers of persistent pain in inflammatory arthritis
Taams, L. (Primary Investigator), Denk, F. (Co-Investigator) & McMahon, S. (Co-Investigator)
26/09/2022 → 25/09/2027
Project: Research