---
title: "Persistent anti-ganglioside autoantibodies in recovered Guillain-Barré syndrome show reduced neuro"
id: "biorxiv-1-autoantibodies-from-recovered-guillain-barre-syndrome-patients-exhibit-altered"
canonical_url: "https://medichelpline.com/clinical-feed/biorxiv-1-autoantibodies-from-recovered-guillain-barre-syndrome-patients-exhibit-altered"
content_type: "clinical_feed_article"
specialty: "Neurology"
source_name: "bioRxiv (Biomedical Preprints)"
source_url: "https://www.biorxiv.org/content/10.64898/2026.08.31.748457v1?rss=1"
published_at: "2026-09-04T12:00:00.000Z"
evidence_level: "Verified Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Persistent anti-ganglioside autoantibodies in recovered Guillain-Barré syndrome show reduced neuro
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/biorxiv-1-autoantibodies-from-recovered-guillain-barre-syndrome-patients-exhibit-altered
- **Specialty:** [Neurology](https://medichelpline.com/clinical-feed/neurology.md)
- **Primary Source:** bioRxiv (Biomedical Preprints)
- **Source URL:** [Original Journal Publication](https://www.biorxiv.org/content/10.64898/2026.08.31.748457v1?rss=1)
- **Published At:** 2026-09-04T12:00:00.000Z
- **Evidence Rating:** Verified Feed
## Executive GIST (TL;DR)
- Guillain-Barré syndrome (GBS) is an autoimmune polyneuropathy often triggered by infection, most commonly **Campylobacter jejuni**, through anti-ganglioside antibodies that cross-react with neuronal gangliosides. - In most patients, neuropathy resolves as anti-ganglioside antibody titers decline and immune stimulation wanes. - The study found that approximately **10%** of clinically confirmed GBS patients retained high circulating anti-ganglioside antibody titers more than a decade after clinical recovery. - Despite persistent titers, sera from recovered patients did not induce neuropathy in a human pluripotent stem cell-derived sensory neuron model when tested with human complement, in contrast to paired acute-phase sera from the same patients. - Comparative analyses of paired acute and recovered sera revealed changes in **IgG** subclass distribution and antibody glycoforms between disease and recovery. - Isolated anti-GM1 ganglioside antibodies from recovered patients showed **anti-inflammatory glycoform modifications**, distinguishing them from pathogenic acute-phase antibodies. - The data support a model in which patients selectively maintain **non-pathogenic variants of autoantibodies** that lack neuron-damaging effector functions but could retain protective activity against C. jejuni. - Methods reported include use of paired acute and recovered sera and a human stem cell-derived sensory neuron plus human complement assay to assess neurotoxic potential. - Funding sources and competing interests were disclosed; specific institutional or experimental protocol details beyond those reported were not provided in the source.
## Clinical Analysis & Structured Key Points
Autoantibodies from recovered Guillain-Barre syndrome patients exhibit altered effector functions that prevent subsequent neuron degeneration | bioRxiv Skip to main content New Results Autoantibodies from recovered Guillain-Barre syndrome patients exhibit altered effector functions that prevent subsequent neuron degeneration Ashley M Rogers , Jessica L McAlpine , Xu Yang , Israt Jahan , Nowshin Papri , Shoma Hayat , Stephanie A Archer-Hartmann , Meagan Shinn , Parastoo Azadi , Nadja Zeltner , Zhahirul Islam , View ORCID Profile Christine M Szymanski doi: https://doi.org/10.64898/2026.08.31.748457 Ashley M Rogers 1 University of Georgia; Find this author on Google Scholar Find this author on PubMed Search for this author on this site Jessica L McAlpine 1 University of Georgia; Find this author on Google Scholar Find this author on PubMed Search for this author on this site Xu Yang 1 University of Georgia; Find this author on Google Scholar Find this author on PubMed Search for this author on this site Israt Jahan 2 icddr,b Find this author on Google Scholar Find this author on PubMed Search for this author on this site Nowshin Papri 2 icddr,b Find this author on Google Scholar Find this author on PubMed Search for this author on this site Shoma Hayat 2 icddr,b Find this author on Google Scholar Find this author on PubMed Search for this author on this site Stephanie A Archer-Hartmann 1 University of Georgia; Find this author on Google Scholar Find this author on PubMed Search for this author on this site Meagan Shinn 1 University of Georgia; Find this author on Google Scholar Find this author on PubMed Search for this author on this site Parastoo Azadi 1 University of Georgia; Find this author on Google Scholar Find this author on PubMed Search for this author on this site Nadja Zeltner 1 University of Georgia; Find this author on Google Scholar Find this author on PubMed Search for this author on this site Zhahirul Islam 2 icddr,b Find this author on Google Scholar Find this author on PubMed Search for this author on this site Christine M Szymanski 1 University of Georgia; Find this author on Google Scholar Find this author on PubMed Search for this author on this site ORCID record for Christine M Szymanski For correspondence: cszymans{at}uga.edu Abstract Info/History Metrics Supplementary material Preview PDF Abstract Guillain-Barre syndrome (GBS) is an autoimmune polyneuropathy that is the leading cause of nonpoliovirus-associated acute flaccid paralysis worldwide. In most cases, GBS occurs following an infection, most commonly Campylobacter jejuni, through the induction of antibodies recognizing bacterial ganglioside-mimicking lipooligosaccharides that cross-react with human neuronal gangliosides. This post-infectious autoimmune cascade causes neuropathy, from which patients can recover as their anti-ganglioside antibody titers diminish and immunostimulation decreases. In this study, we find 10% of clinically confirmed GBS patients maintain high titers of circulating anti-ganglioside antibodies more than one decade after recovery. These antibodies no longer cause neuropathy compared to acute sera from the same patients using a human pluripotent stem cell-derived sensory neuron model with human complement. We found both IgG subclass and glycoform differences between paired acute and recovered GBS patient sera, including anti-inflammatory modifications on isolated anti-GM1 ganglioside antibodies. Together, these data suggest that patients with GBS select for non-pathogenic variants of autoantibodies that are no longer capable of damaging their neurons, but may still protect against C. jejuni infection. Competing Interest Statement Dr. Zeltner is the founder and owner of Neela Cell Therapeutics, LLC. All other authors declare no competing interests. Funder Information Declared United States Department of Defense , PR191209 National Institutes of Health , R21AI175925 , 5T32GM145 , R24GM137782 Copyright The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC 4.0 International license . Back to top Previous Next Posted September 04, 2026. Download PDF Supplementary Material Email Thank you for your interest in spreading the word about bioRxiv. NOTE: Your email address is requested solely to identify you as the sender of this article. 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Share Autoantibodies from recovered Guillain-Barre syndrome patients exhibit altered effector functions that prevent subsequent neuron degeneration Ashley M Rogers , Jessica L McAlpine , Xu Yang , Israt Jahan , Nowshin Papri , Shoma Hayat , Stephanie A Archer-Hartmann , Meagan Shinn , Parastoo Azadi , Nadja Zeltner , Zhahirul Islam , Christine M Szymanski bioRxiv 2026.08.31.748457; doi: https://doi.org/10.64898/2026.08.31.748457 Share This Article: Copy Citation Tools Autoantibodies from recovered Guillain-Barre syndrome patients exhibit altered effector functions that prevent subsequent neuron degeneration Ashley M Rogers , Jessica L McAlpine , Xu Yang , Israt Jahan , Nowshin Papri , Shoma Hayat , Stephanie A Archer-Hartmann , Meagan Shinn , Parastoo Azadi , Nadja Zeltner , Zhahirul Islam , Christine M Szymanski bioRxiv 2026.08.31.748457; doi: https://doi.org/10.64898/2026.08.31.748457 Citation Manager Formats BibTeX Bookends EasyBib EndNote (tagged) EndNote 8 (xml) Medlars Mendeley Papers RefWorks Tagged Ref Manager RIS Zotero Tweet Widget Facebook Like Google Plus One Subject Areas All Articles Animal Behavior and Cognition (7962) Biochemistry (18614) Bioengineering (14760) Bioinformatics (44108) Biophysics (22441) Cancer Biology (19580) Cell Biology (26727) Clinical Trials (138) Developmental Biology (13895) Ecology (20878) Epidemiology (2067) Evolutionary Biology (25307) Genetics (16093) Genomics (23382) Immunology (18587) Microbiology (42208) Molecular Biology (17937) Neuroscience (92823) Paleontology (693) Pathology (2967) Pharmacology and Toxicology (5060) Physiology (8054) Plant Biology (15897) Scientific Communication and Education (2091) Synthetic Biology (4536) Systems Biology (10180) Zoology (2375)
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