ArticleBrain, behavior, and immunity2025
Reducing IgG accumulation via neonatal Fc receptor (FcRn) blockade relieves neuropathic pain.
Article in Brain, behavior, and immunity, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- TRPM2 is a direct pain transducer.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Recent advances in autoantibody-mediated pain.Current opinion in supportive and palliative care · 2026Review
- Targeting FcRn for immunomodulation: a promising therapy in autoimmune inflammatory rheumatic diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Autoantibodies as drivers of neuropathic pain.Trends in molecular medicine · 2026Review
- Perinatal Antibiotic Timing Impairs Maternal IgG Transfer via FcRn and Shapes the Neonatal Gut Microbiome in Mice.Microorganisms · 2026Article
- Peripheral nerve injury reduces macrophage efferocytosis to facilitate neuropathic pain.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Neuroinflammation as a failure of allostatic integrity: a hierarchical-circular model of biological memory for pathogenesis in neurodegenerative and neuropsychiatric diseases.Frontiers in systems neuroscience · 2026Article
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- Pharmacovigilance analysis of FcRn antagonists in the treatment of myasthenia gravis: A disproportionality analysis based on the FAERS database.Human vaccines & immunotherapeutics · 2025Article
- Neural Immunoglobulins Shape Brain Circuits.The European journal of neuroscience · 2025Review
- Fc gamma receptor IIa signaling from spinal cord astrocytes promotes neuropathic pain in rats.The journal of pain · 2025Article
- Pain in systemic lupus erythematosus: emerging insights and paradigms.Nature reviews. Rheumatology · 2025Review
- Ectopic Nociceptor Sprouting as a Key Peripheral Driver of Pain in Rheumatoid Arthritis.Current rheumatology reports · 2025Review
- Blockade of IgG Fc receptors reduces pain after intervertebral disc injury.Pharmacological reports : PR · 2025Article
- A unified spectrum model for the anti-GQ1b antibody syndromes: from pathophysiology to a new diagnostic framework.Frontiers in neurologyReview
- The impact of nerve injury on the immune system across the lifespan is sexually dimorphic.Neurobiology of pain (Cambridge, Mass.)Article
- Sex differences in nerve injury-induced neuropathic pain via REST in primary sensory neurons.Neurobiology of pain (Cambridge, Mass.)Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Preclinical and clinical studies have established that autoreactive immunoglobulin G (IgG) can drive neuropathic pain. We recently demonstrated that sciatic nerve chronic constriction injury (CCI) in male and female mice results in the production of pronociceptive IgG, which accumulates around the lumbar region, including within the dorsal root ganglia (DRG) and spinal cord, facilitating the development of neuropathic pain. These data raise the intriguing possibility that neuropathic pain may be alleviated by reducing the accumulation of IgG. To this end, we tested whether biologic inhibition or genetic deletion of the neonatal Fc receptor (FcRn) would attenuate mechanical hypersensitivity (allodynia) and IgG deposition induced by CCI. FcRn are prominently expressed on myeloid and endothelial cells and extend the half-life of IgG via pinocytosis and recycling into the extracellular milieu. We show here that administration of the FcRn blocker efgartigimod either 7- or 28-days post-CCI relieved allodynia among both male and female mice, compared to the Fc fragment control. Efgartigimod, administered systemically (intraperitoneal) or to the lumbar region (intrathecal), attenuated mechanical allodynia for at least one month. CCI-induced allodynia was similarly reduced in FcRn-deficient (FcRn
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Registered trials
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 Socratic graph.