An interdisciplinary perspective on peripheral drivers of pain in rheumatoid arthritis.

Autor: Rutter-Locher Z; Department of Rheumatology, Guy's Hospital, London, UK.; Centre for Inflammation Biology & Cancer Immunology, Department of Inflammation Biology, School of Immunology & Microbial Sciences, King's College London, London, UK., Kirkham BW; Department of Rheumatology, Guy's Hospital, London, UK., Bannister K; Wolfson Sensory Pain and Regeneration Centre (SPaRC), King's College London, London, UK., Bennett DL; Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK., Buckley CD; Kennedy Institute for Rheumatology, University of Oxford, Oxford, UK., Taams LS; Centre for Inflammation Biology & Cancer Immunology, Department of Inflammation Biology, School of Immunology & Microbial Sciences, King's College London, London, UK. leonie.taams@kcl.ac.uk., Denk F; Wolfson Sensory Pain and Regeneration Centre (SPaRC), King's College London, London, UK. franziska.denk@kcl.ac.uk.
Jazyk: angličtina
Zdroj: Nature reviews. Rheumatology [Nat Rev Rheumatol] 2024 Nov; Vol. 20 (11), pp. 671-682. Date of Electronic Publication: 2024 Sep 06.
DOI: 10.1038/s41584-024-01155-z
Abstrakt: 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.
(© 2024. Springer Nature Limited.)
Databáze: MEDLINE
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