{
  "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.",
  "abstract_shown": true,
  "affiliations": [
    "University of Georgia"
  ],
  "article_type": "New results",
  "arxiv": null,
  "author_total": 12,
  "authors": [
    {
      "name": "A. M. Rogers"
    },
    {
      "name": "J. L. McAlpine"
    },
    {
      "name": "X. Yang"
    },
    {
      "name": "I. Jahan"
    },
    {
      "name": "N. Papri"
    },
    {
      "name": "S. Hayat"
    },
    {
      "name": "S. A. Archer-Hartmann"
    },
    {
      "name": "M. Shinn"
    },
    {
      "name": "P. Azadi"
    },
    {
      "name": "N. Zeltner"
    },
    {
      "name": "Z. Islam"
    },
    {
      "affs": [
        0
      ],
      "name": "C. M. Szymanski"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/4kyd6bweynnmj.bib",
  "cited_by": 0,
  "doi": "10.64898/2026.08.31.748457",
  "fulltext_url": "https://www.biorxiv.org/content/10.64898/2026.08.31.748457v1.full",
  "id": "4kyd6bweynnmj",
  "issns": [],
  "landing_url": "https://www.biorxiv.org/content/10.64898/2026.08.31.748457v1",
  "language": null,
  "licence": "CC-BY-NC",
  "licence_label": "CC BY-NC",
  "licence_source": "article",
  "licence_url": "https://creativecommons.org/licenses/by-nc/4.0/",
  "metadata_licence": null,
  "native_subjects": [
    [
      "biorxiv",
      "immunology"
    ],
    [
      "openalex",
      "2728|Peripheral Neuropathies and Disorders"
    ]
  ],
  "openalex": "W7208835717",
  "pdf_url": "https://www.biorxiv.org/content/10.64898/2026.08.31.748457v1.full.pdf",
  "pmcid": null,
  "pmid": null,
  "published": "2026-08-31",
  "publisher": null,
  "ris": "https://research.draconitic.com/paper/4kyd6bweynnmj.ris",
  "sources": [
    {
      "first_seen": "2026-10-30T12:19:33Z",
      "native_id": "10.64898/2026.08.31.748457",
      "source": "biorxiv",
      "url": "https://www.biorxiv.org/content/10.64898/2026.08.31.748457v1"
    }
  ],
  "subjects": [
    {
      "field": "biology",
      "origin": "biorxiv:immunology",
      "subfield": "immunology"
    }
  ],
  "title": "Autoantibodies from recovered Guillain-Barre syndrome patients exhibit altered effector functions that prevent subsequent neuron degeneration",
  "title_text": "Autoantibodies from recovered Guillain-Barre syndrome patients exhibit altered effector functions that prevent subsequent neuron degeneration",
  "type": "preprint",
  "updated_at": "2026-10-30T12:19:33Z",
  "url": "https://research.draconitic.com/paper/4kyd6bweynnmj",
  "venue": "bioRxiv",
  "versions": []
}