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https://journals.lww.com/painrpts/f...mediated_autoimmunity_in_symptom_based.4.aspx
MEETING PROCEEDINGS
Antibody-mediated autoimmunity in symptom-based disorders: position statement and proceedings from an international workshop
A 2-day closed workshop was held in Liverpool, United Kingdom, to discuss the results of research concerning symptom-based disorders (SBDs) caused by autoantibodies, share technical knowledge, and consider future plans. Twenty-two speakers and 14 additional participants attended.
This workshop set out to consolidate knowledge about the contribution of autoantibodies to SBDs.
Persuasive evidence for a causative role of autoantibodies in disease often derives from experimental “passive transfer” approaches, as first established in neurological research. Here, serum immunoglobulin (IgM or IgG) is purified from donated blood and transferred to rodents, either systemically or intrathecally.
Rodents are then assessed for the expression of phenotypes resembling the human condition; successful phenotype transfer is considered supportive of or proof for autoimmune pathology.
Workshop participants discussed passive transfer models and wider evidence for autoantibody contribution to a range of SBDs.
Clinical trials testing autoantibody reduction were presented.
Cornerstones of both experimental approaches and clinical trial parameters in this field were distilled and presented in this article.
Mounting evidence suggests that immunoglobulin transfer from patient donors often induces the respective SBD phenotype in rodents.
Understanding antibody binding epitopes and downstream mechanisms will require substantial research efforts, but treatments to reduce antibody titres can already now be evaluated.
https://journals.lww.com/painrpts/f...mediated_autoimmunity_in_symptom_based.4.aspx
MEETING PROCEEDINGS
Antibody-mediated autoimmunity in symptom-based disorders: position statement and proceedings from an international workshop
AbstractMountford, Rebeccaa,*; Adler, Brittany L.b; Andersson, Davidc; Bashford-Rogers, Rachaeld; Berwick, Richarda,c; Bevan, Stuartc; Caro, Xaviere; Chung, Tae Hwanf,g; Clark, J. Davidh; Dawes, John M.i; Dong, Xinzhongj; Helyes, Zsuzsannak,l,m; Kingery, Waden; van Middendorp, Joost J.o; Neiland, Harveya; Maurer, Margotc; Scheibenbogen, Carmenp; Schmack, Katharinaq,r; Schreiner, Thomass; Svensson, Camilla I.t; Tékus, Valériak,u; Goebel, Andreasa,v
Author Information
aPain Research Institute, University of Liverpool, Liverpool, United Kingdom
bDivision of Rheumatology, Johns Hopkins University, Baltimore, MD, USA
cWolfson SPaRC, Institute of Psychiatry, Psychology & Neuroscience, King's College London, London, United Kingdom
dDepartment of Biochemistry, University of Oxford, Oxford, United Kingdom
eSouthern California Fibromyalgia Research & Treatment Centre, Northridge Hospital Medical Center Professional Building, Los Angeles, CA, USA
fDepartment of Physical Medicine and Rehabilitation, The Johns Hopkins Medical Institutions, Baltimore, MD, USA
gDepartment of Neurology, The Johns Hopkins Medical Institutions, Baltimore, MD, USA
hDepartment of Anesthesia, Stanford University School of Medicine, Redwood City, CA, USA
iNuffield Department of Clinical Neurosciences, University of Oxford, Oxford, United Kingdom
jSolomon H. Snyder Department of Neuroscience, John Hopkins University School of Medicine, Baltimore, MD, USA
kDepartment of Pharmacology and Pharmacotherapy, Medial School, University of Pécs, Pécs, Hungary
lHUNREN-PTE Chronic Pain Research Group, University of Pécs, Pécs, Hungary
mPharmInVivo Ltd., Pécs, Hungary
nPalo Alto Veterans Institute for Research, Palo Alto, CA, USA
oArgenx, Ghent, Belgium
pInstitute of Medical Immunology, Charité—Universitätsmedizin Berlin, Berlin Institute of Health, Berlin, Germany
qFrancis Crick Institute, London, United Kingdom
rDivision of Psychiatry, University College London, London, United Kingdom
sMiltenyi Biotec, Bergisch Gladbach, Germany
tDepartment of Physiology and Pharmacology, Centre for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden
uDepartment of Laboratory Diagnostics, University of Pécs, Pécs, Hungary
vWalton Centre NHS Foundation Trust, Liverpool, United Kingdom
*Corresponding author. Address: Pain Research Institute, University of Liverpool, Liverpool, L9 7AL United Kingdom. Tel.: 0151 529 5835. E-mail address: r.mountford@liverpool.ac.uk (R. Mountford).
Sponsorships or competing interests that may be relevant to content are disclosed at the end of this article.
This is an open access article distributed under the Creative Commons Attribution-NoDerivatives License 4.0 (CC BY-ND) which allows for redistribution, commercial and non-commercial, as long as it is passed along unchanged and in whole, with credit to the author.
PAIN Reports 9(4)e1167, August 2024. | DOI: 10.1097/PR9.0000000000001167
- OPEN
A 2-day closed workshop was held in Liverpool, United Kingdom, to discuss the results of research concerning symptom-based disorders (SBDs) caused by autoantibodies, share technical knowledge, and consider future plans. Twenty-two speakers and 14 additional participants attended.
This workshop set out to consolidate knowledge about the contribution of autoantibodies to SBDs.
Persuasive evidence for a causative role of autoantibodies in disease often derives from experimental “passive transfer” approaches, as first established in neurological research. Here, serum immunoglobulin (IgM or IgG) is purified from donated blood and transferred to rodents, either systemically or intrathecally.
Rodents are then assessed for the expression of phenotypes resembling the human condition; successful phenotype transfer is considered supportive of or proof for autoimmune pathology.
Workshop participants discussed passive transfer models and wider evidence for autoantibody contribution to a range of SBDs.
Clinical trials testing autoantibody reduction were presented.
Cornerstones of both experimental approaches and clinical trial parameters in this field were distilled and presented in this article.
Mounting evidence suggests that immunoglobulin transfer from patient donors often induces the respective SBD phenotype in rodents.
Understanding antibody binding epitopes and downstream mechanisms will require substantial research efforts, but treatments to reduce antibody titres can already now be evaluated.
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