ReviewPain reports2021
Autoimmune regulation of chronic pain.
Review in Pain reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis 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
36 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Comparative transcriptomic meta-analysis reveals elevated TCL1A expression in human circulating immune cells across chronic pain conditions.British journal of anaesthesia · 2026Pooled it
- Home-based respiratory-gated transcutaneous auricular vagus nerve stimulation for rheumatoid arthritis-a feasibility study.Clinical rheumatology · 2026Trial
- 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
- Article
- Pathogenic IgG from long COVID patients with neurological sequelae triggers sensitive but not cognitive impairments upon transfer into mice.Acta neuropathologica · 2026Article
- Comprehensive antigen profiling predicts post-surgical neuropathic pain in women treated for breast cancer.Scientific reports · 2026Article
- Neuroimmune interactions in arthritis: linking pain sensitisation and inflammation.Journal of bone and mineral metabolism · 2026Review
- Article
- C-Reactive Protein and Neurological Autoimmune Diseases: Bridging the Diagnostic and Pathogenic Gap.International journal of molecular sciences · 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
- Article
- Fc gamma receptor IIa signaling from spinal cord astrocytes promotes neuropathic pain in rats.The journal of pain · 2025Article
- Article
- Pain in systemic lupus erythematosus: emerging insights and paradigms.Nature reviews. Rheumatology · 2025Review
- Pathogenic Crosstalk Between the Peripheral and Central Nervous System in Rheumatic Diseases: Emerging Evidence and Clinical Implications.International journal of molecular sciences · 2025Review
- Reducing IgG accumulation via neonatal Fc receptor (FcRn) blockade relieves neuropathic pain.Brain, behavior, and immunity · 2025Article
- Caveolin-1 knockout improves CFA-induced inflammatory pain in adult mice through modulating the cGAS STING pathway and autophagy.PloS one · 2025Article
- Transcriptome analysis of rheumatoid arthritis uncovers genes linked to inflammation-induced pain.Scientific reports · 2024Article
- B cells drive neuropathic pain-related behaviors in mice through IgG-Fc gamma receptor signaling.Science translational medicine · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic pain is an unpleasant and debilitating condition that is often poorly managed by existing therapeutics. Reciprocal interactions between the nervous system and the immune system have been recognized as playing an essential role in the initiation and maintenance of pain. In this review, we discuss how neuroimmune signaling can contribute to peripheral and central sensitization and promote chronic pain through various autoimmune mechanisms. These pathogenic autoimmune mechanisms involve the production and release of autoreactive antibodies from B cells. Autoantibodies-ie, antibodies that recognize self-antigens-have been identified as potential molecules that can modulate the function of nociceptive neurons and thereby induce persistent pain. Autoantibodies can influence neuronal excitability by activating the complement pathway; by directly signaling at sensory neurons expressing Fc gamma receptors, the receptors for the Fc fragment of immunoglobulin G immune complexes; or by binding and disrupting ion channels expressed by nociceptors. Using examples primarily from rheumatoid arthritis, complex regional pain syndrome, and channelopathies from potassium channel complex autoimmunity, we suggest that autoantibody signaling at the central nervous system has therapeutic implications for designing novel disease-modifying treatments for chronic pain.
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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.