ArticleScience translational medicine2024
B cells drive neuropathic pain-related behaviors in mice through IgG-Fc gamma receptor signaling.
Article in Science translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 2 of them syntheses that pooled it.
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Who cites it
46 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Sexually Dimorphic Neuroimmune Pathways in Chronic Pain: A Comprehensive Systematic Review of Cellular and Molecular Mechanisms.Biomolecules · 2026Pooled it
- Comparative transcriptomic meta-analysis reveals elevated TCL1A expression in human circulating immune cells across chronic pain conditions.British journal of anaesthesia · 2026Pooled it
- T cell-dependent modulation of pain behaviors in a rat model of recurring paclitaxel-induced peripheral neuropathy.Brain, behavior, & immunity - health · 2026Article
- 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
- Compartmentalized B cell-microglia crosstalk drives ischemic white matter demyelination.Nature communications · 2026Article
- Inflammatory neuropathy in mouse and primate models of colorectal cancer.Nature communications · 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
- Piezo2 Mediates a Vicious Cycle of "Mechanical Homeostasis Imbalance-Inflammation" in Sensory Nerves and the Cartilage Endplate.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- C-C motif chemokine ligand 12 (CCL12) is a critical chemokine driving postoperative pain.Pain · 2026Article
- Pathogenic IgG from long COVID patients with neurological sequelae triggers sensitive but not cognitive impairments upon transfer into mice.Acta neuropathologica · 2026Article
- Pathogenic Role of FGFR3 Autoantibodies in Small Fiber Neuropathy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Human pain transcriptomics: lessons learned so far.Pain reports · 2026Review
- Immuno-Inflammatory Mechanisms in the Chronification of Pain.Pain and therapy · 2026Review
- Comprehensive antigen profiling predicts post-surgical neuropathic pain in women treated for breast cancer.Scientific reports · 2026Article
- Roles of the Complement System in Peripheral Nerve Injury and Repair.Bioengineering (Basel, Switzerland) · 2026Review
- Article
- Autoantibodies as drivers of neuropathic pain.Trends in molecular medicine · 2026Review
- Peripheral nerve injury reduces macrophage efferocytosis to facilitate neuropathic pain.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Dorsal Root Ganglion as a Hub for Peripheral Sensitization: A Hierarchical Regulation Model and Translational Progress.Journal of pain research · 2026Review
Corrections and comments
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Authors and funding
24 authors.
Funding
Abstract
Neuroimmune interactions are essential for the development of neuropathic pain, yet the contributions of distinct immune cell populations have not been fully unraveled. Here, we demonstrate the critical role of B cells in promoting mechanical hypersensitivity (allodynia) after peripheral nerve injury in male and female mice. Depletion of B cells with a single injection of anti-CD20 monoclonal antibody at the time of injury prevented the development of allodynia. B cell-deficient (muMT) mice were similarly spared from allodynia. Nerve injury was associated with increased immunoglobulin G (IgG) accumulation in ipsilateral lumbar dorsal root ganglia (DRGs) and dorsal spinal cords. IgG was colocalized with sensory neurons and macrophages in DRGs and microglia in spinal cords. IgG also accumulated in DRG samples from human donors with chronic pain, colocalizing with a marker for macrophages and satellite glia. RNA sequencing revealed a B cell population in naive mouse and human DRGs. A B cell transcriptional signature was enriched in DRGs from human donors with neuropathic pain. Passive transfer of IgG from injured mice induced allodynia in injured muMT recipient mice. The pronociceptive effects of IgG are likely mediated through immune complexes interacting with Fc gamma receptors (FcγRs) expressed by sensory neurons, microglia, and macrophages, given that both mechanical allodynia and hyperexcitability of dissociated DRG neurons were abolished in nerve-injured FcγR-deficient mice. Consistently, the pronociceptive effects of IgG passive transfer were lost in FcγR-deficient mice. These data reveal that a B cell-IgG-FcγR axis is required for the development of neuropathic pain in mice.
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