Autoantibodies from recovered Guillain-Barre syndrome patients exhibit altered effector functions that prevent subsequent neuron degeneration
- 1University of Georgia
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.
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BibTeX
@misc{rogers2026autoantibodies,
title = {{Autoantibodies from recovered Guillain-Barre syndrome patients exhibit altered effector functions that prevent subsequent neuron degeneration}},
author = {A. M. Rogers and J. L. McAlpine and X. Yang and I. Jahan and N. Papri and S. Hayat and S. A. Archer-Hartmann and M. Shinn and P. Azadi and N. Zeltner and Z. Islam and C. M. Szymanski},
howpublished = {bioRxiv},
year = {2026},
month = aug,
doi = {10.64898/2026.08.31.748457},
url = {https://www.biorxiv.org/content/10.64898/2026.08.31.748457v1},
note = {CC BY-NC},
}
RIS
TY - UNPB
TI - Autoantibodies from recovered Guillain-Barre syndrome patients exhibit altered effector functions that prevent subsequent neuron degeneration
AU - A. M. Rogers
AU - J. L. McAlpine
AU - X. Yang
AU - I. Jahan
AU - N. Papri
AU - S. Hayat
AU - S. A. Archer-Hartmann
AU - M. Shinn
AU - P. Azadi
AU - N. Zeltner
AU - Z. Islam
AU - C. M. Szymanski
PY - 2026
DA - 2026/08/31
PB - bioRxiv
DO - 10.64898/2026.08.31.748457
UR - https://www.biorxiv.org/content/10.64898/2026.08.31.748457v1
AB - 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.
ER -