ArticleThe Journal of clinical investigation2019
Neuronal FcγRI mediates acute and chronic joint pain.
Article in The Journal of clinical investigation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 57 citations in OpenAlex.
- MARCH2/3 target FcγRI for K27-linked polyubiquitination and degradation to restrict the inflammatory response.Cellular & molecular immunology · 2026Article
- TRPM2 is a direct pain transducer.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Inhibition of Janus kinase/signal transducer and activator of transcription reduces nociceptive sensitization in a murine model of complex regional pain syndrome.Pain reports · 2026Article
- Clinical outcomes in psoriatic arthritis patients with rheumatoid factor positivity.Rheumatology (Oxford, England) · 2026Article
- Human pain transcriptomics: lessons learned so far.Pain reports · 2026Review
- Pathogenic Drivers of Difficult-to-Treat Rheumatoid Arthritis: Synovium and Beyond.International journal of molecular sciences · 2026Review
- Mast cell-expressed Mrgprb2/MRGPRX2 mediates gout pain and inflammation via a neuroimmune axis.JCI insight · 2026Article
- The neuro-immune insights of itch: peripheral mechanisms and central glial contributions.Cellular & molecular biology letters · 2026Review
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- Preclinical assessment of two FcγRI-specific antibodies that competitively inhibit immune complex-FcγRI binding to suppress autoimmune responses.Nature communications · 2025Article
- Fc gamma receptor IIa signaling from spinal cord astrocytes promotes neuropathic pain in rats.The journal of pain · 2025Article
- Blockade of IgG Fc receptors reduces pain after intervertebral disc injury.Pharmacological reports : PR · 2025Article
- Reducing IgG accumulation via neonatal Fc receptor (FcRn) blockade relieves neuropathic pain.Brain, behavior, and immunity · 2025Article
- Pain mechanism and management strategy of rheumatoid arthritis.Frontiers in pain research (Lausanne, Switzerland) · 2025Review
- Commentary: Guselkumab binding to CD64Frontiers in immunology · 2025Article
- Autoantibodies cause nociceptive sensitization in a mouse model of degenerative osteoarthritis.Pain · 2024Article
- Transcriptome analysis of rheumatoid arthritis uncovers genes linked to inflammation-induced pain.Scientific reports · 2024Article
- The influence of sex on neuroimmune communication, pain, and physiology.Biology of sex differences · 2024Review
- B cells drive neuropathic pain-related behaviors in mice through IgG-Fc gamma receptor signaling.Science translational medicine · 2024Article
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Although joint pain in rheumatoid arthritis (RA) is conventionally thought to result from inflammation, arthritis pain and joint inflammation are at least partially uncoupled. This suggests that additional pain mechanisms in RA remain to be explored. Here we show that FcγRI, an immune receptor for IgG immune complex (IgG-IC), is expressed in a subpopulation of joint sensory neurons and that, under naïve conditions, FcγRI crosslinking by IgG-IC directly activates the somata and peripheral terminals of these neurons to evoke acute joint hypernociception without obvious concurrent joint inflammation. These effects were diminished in both global and sensory neuron-specific Fcgr1 knockout mice. In murine models of inflammatory arthritis, FcγRI signaling was upregulated in joint sensory neurons. Acute blockade or global genetic deletion of Fcgr1 significantly attenuated arthritis pain and hyperactivity of joint sensory neurons without measurably altering joint inflammation. Conditional deletion of Fcgr1 in sensory neurons produced similar analgesic effects in these models. We therefore suggest that FcγRI expressed in sensory neurons contributes to arthritis pain independently of its functions in inflammatory cells. These findings expand our understanding of the immunosensory capabilities of sensory neurons and imply that neuronal FcγRI merits consideration as a target for treating RA pain.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.