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.

Zoe Rutter-Locher

Bruce W Kirkham

Kirsty Bannister

David L Bennett

Christopher D Buckley

Leonie S Taams

Franziska Denk

Nature Reviews Rheumatology

期刊范围涵盖风湿病研究的整个范围。我们确保我们的文章可供最广泛的受众访问。

Nature Reviews Rheumatology covers the entire spectrum of rheumatology research. We are committed to ensuring that our articles are accessible to the widest possible audience.

《Nature Reviews Rheumatology》期刊涵盖了风湿病研究的各个领域。我们致力于确保我们的文章能够被最广泛的受众所访问。

Category	Quartile
医学	1
医学, 风湿病学	1

An interdisciplinary perspective on peripheral drivers of pain in rheumatoid arthritis

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