Evidence map›Paper›PMID 34196305›Full record

ArticleThe Journal of clinical investigation2021

Passive transfer of fibromyalgia symptoms from patients to mice.

Andreas Goebel, Emerson Krock, Clive Gentry, Mathilde R Israel, Alexandra Jurczak, Carlos Morado Urbina, Katalin Sandor, Nisha Vastani, Margot Maurer, Ulku Cuhadar and 13 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 157 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
157citing papers in PubMed, 1 pooled it
24.4field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

157 citing papers in PubMed, 1 synthesis or guideline pooled it, 245 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Glial cells in neuropathic pain.Physiological reviews · 2026
    Review
  5. TRPM2 is a direct pain transducer.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  6. Review
  7. Fibromyalgia: a real phantom pain?Clinical rheumatology · 2026
    Review
  8. Article
  9. Recent advances in autoantibody-mediated pain.Current opinion in supportive and palliative care · 2026
    Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Fibromyalgia: A Multifactorial Pain Disorder.International journal of molecular sciences · 2026
    Review
  17. Article
  18. Article
  19. Article
  20. Review

97 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

23 authors at 5 institutions in 3 countries.

Andreas GoebelWalton Centre NHS Foundation Trust, Liverpool, United Kingdom.
Emerson KrockDepartment of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
Clive GentryKing's College London, Wolfson CARD, Institute of Psychiatry, Psychology & Neuroscience, Guy's Campus, London, United Kingdom.
Mathilde R IsraelKing's College London, Wolfson CARD, Institute of Psychiatry, Psychology & Neuroscience, Guy's Campus, London, United Kingdom.
Alexandra JurczakDepartment of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
Carlos Morado UrbinaDepartment of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
Katalin SandorDepartment of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
Nisha VastaniKing's College London, Wolfson CARD, Institute of Psychiatry, Psychology & Neuroscience, Guy's Campus, London, United Kingdom.
Margot MaurerKing's College London, Wolfson CARD, Institute of Psychiatry, Psychology & Neuroscience, Guy's Campus, London, United Kingdom.
Ulku CuhadarKing's College London, Wolfson CARD, Institute of Psychiatry, Psychology & Neuroscience, Guy's Campus, London, United Kingdom.
Serena SensiPain Research Institute, Institute of Life Course and Medical Sciences, University of Liverpool, Liverpool, United Kingdom.
Yuki NomuraDepartment of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
Joana MenezesDepartment of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
Azar BaharpoorDepartment of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
Louisa BrieskornDepartment of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
Angelica SandströmDepartment of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
Jeanette TourDepartment of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
Diana KadetoffDepartment of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
Lisbet HaglundDepartment of Surgery, Division of Orthopaedic Surgery, McGill University, Montreal, Quebec, Canada.
Eva KosekDepartment of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
Stuart BevanKing's College London, Wolfson CARD, Institute of Psychiatry, Psychology & Neuroscience, Guy's Campus, London, United Kingdom.
Camilla I SvenssonDepartment of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
David A AnderssonKing's College London, Wolfson CARD, Institute of Psychiatry, Psychology & Neuroscience, Guy's Campus, London, United Kingdom.
Karolinska Institutet · SEKing's College London · GBUniversity of Liverpool · GBMcGill University · CAUppsala University · SE

Funding

CIHR MFE-171299Medical Research Council MR/S003428/1Versus Arthritis 21543Versus Arthritis 21544
6 · The paper itself

Abstract

Fibromyalgia syndrome (FMS) is characterized by widespread pain and tenderness, and patients typically experience fatigue and emotional distress. The etiology and pathophysiology of fibromyalgia are not fully explained and there are no effective drug treatments. Here we show that IgG from FMS patients produced sensory hypersensitivity by sensitizing nociceptive neurons. Mice treated with IgG from FMS patients displayed increased sensitivity to noxious mechanical and cold stimulation, and nociceptive fibers in skin-nerve preparations from mice treated with FMS IgG displayed an increased responsiveness to cold and mechanical stimulation. These mice also displayed reduced locomotor activity, reduced paw grip strength, and a loss of intraepidermal innervation. In contrast, transfer of IgG-depleted serum from FMS patients or IgG from healthy control subjects had no effect. Patient IgG did not activate naive sensory neurons directly. IgG from FMS patients labeled satellite glial cells and neurons in vivo and in vitro, as well as myelinated fiber tracts and a small number of macrophages and endothelial cells in mouse dorsal root ganglia (DRG), but no cells in the spinal cord. Furthermore, FMS IgG bound to human DRG. Our results demonstrate that IgG from FMS patients produces painful sensory hypersensitivities by sensitizing peripheral nociceptive afferents and suggest that therapies reducing patient IgG titers may be effective for fibromyalgia.

Indexed as

AnimalsCase-Control StudiesDisease Models, AnimalFemaleFibromyalgiaGanglia, SpinalHumansImmunization, PassiveImmunoglobulin GMaleMiceMice, Inbred C57BLNociceptorsPainPain ThresholdImmunoglobulin GAutoimmune diseasesNeurological disordersNeurosciencePain

Identifiers

PMID34196305
PMCPMC8245181
OpenAlexW3174972846

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.