ArticleProceedings of the National Academy of Sciences of the United States of America2019
Transfer of complex regional pain syndrome to mice via human autoantibodies is mediated by interleukin-1-induced mechanisms.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 66 papers, 2 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
66 citing papers in PubMed, 2 syntheses or guidelines pooled it, 118 citations in OpenAlex.
- Complex Regional Pain Syndrome: Practical Diagnostic and Treatment Guidelines, 5th Edition.Pain medicine (Malden, Mass.) · 2022Guideline
- Pooled it
- Recent advances in autoantibody-mediated pain.Current opinion in supportive and palliative care · 2026Review
- Causal relationship between plasma metabolites and chronic regional pain: a Mendelian randomization study.Metabolism open · 2026Article
- Review
- Pathogenic IgG from long COVID patients with neurological sequelae triggers sensitive but not cognitive impairments upon transfer into mice.Acta neuropathologica · 2026Article
- Autonomic Receptor Autoantibodies in Complex Regional Pain Syndrome and Other Chronic Pain Conditions: A Cross-Sectional Analysis.Biomedicines · 2026Article
- Autoantibodies as drivers of neuropathic pain.Trends in molecular medicine · 2026Review
- The neuroimmune axis and chronic pain disorders.iScience · 2026Review
- Nociplastic pain: the prominent role of non-neuronal cells in central and peripheral sensitization.Frontiers in immunology · 2026Review
- Article
- Future healthcare for patients with the common pain disorder 'fibromyalgia syndrome' - fundamental changes based on the discovery of an immune cause.Future healthcare journal · 2025Article
- Fc gamma receptor IIa signaling from spinal cord astrocytes promotes neuropathic pain in rats.The journal of pain · 2025Article
- M2 Macrophages are Major Mediators of Germline Risk of Endometriosis and Explain Pleiotropy With Comorbid Traits.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Neuronal Reg3β/macrophage TNF-α-mediated positive feedback signaling contributes to pain chronicity in a rat model of CRPS-I.Science advances · 2025Article
- [Biomarkers in complex regional pain syndrome].Schmerz (Berlin, Germany) · 2025Review
- The Inflammasome-miR Axis in Alzheimer's Disease and Chronic Pain: Molecular Mechanisms and Therapeutic Opportunities.Aging and disease · 2025Review
- Sex Differences in the Regulation of Interleukins in Chronic Pain: A Widely Recognized but Difficult-to-Tackle Factor.International journal of molecular sciences · 2025Review
- Reducing IgG accumulation via neonatal Fc receptor (FcRn) blockade relieves neuropathic pain.Brain, behavior, and immunity · 2025Article
- Role of microbiota in pain: From bench to bedside.iMetaOmics · 2025Review
6 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
16 authors at 6 institutions in 2 countries.
Funding
Abstract
Neuroimmune interactions may contribute to severe pain and regional inflammatory and autonomic signs in complex regional pain syndrome (CRPS), a posttraumatic pain disorder. Here, we investigated peripheral and central immune mechanisms in a translational passive transfer trauma mouse model of CRPS. Small plantar skin-muscle incision was performed in female C57BL/6 mice treated daily with purified serum immunoglobulin G (IgG) from patients with longstanding CRPS or healthy volunteers followed by assessment of paw edema, hyperalgesia, inflammation, and central glial activation. CRPS IgG significantly increased and prolonged swelling and induced stable hyperalgesia of the incised paw compared with IgG from healthy controls. After a short-lasting paw inflammatory response in all groups, CRPS IgG-injected mice displayed sustained, profound microglia and astrocyte activation in the dorsal horn of the spinal cord and pain-related brain regions, indicating central sensitization. Genetic deletion of interleukin-1 (IL-1) using IL-1αβ knockout (KO) mice and perioperative IL-1 receptor type 1 (IL-1R1) blockade with the drug anakinra, but not treatment with the glucocorticoid prednisolone, prevented these changes. Anakinra treatment also reversed the established sensitization phenotype when initiated 8 days after incision. Furthermore, with the generation of an IL-1β floxed
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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 OpenQuestion graph.