Autoantibodies from recovered Guillain-Barre syndrome patients exhibit altered effector functions that prevent subsequent neuron degeneration

Guillain-Barre syndrome (GBS) is an autoimmune disorder that often follows an infection, most commonly Campylobacter jejuni. This triggers antibodies that resemble bacterial ganglioside-mimicking lipooligosaccharides, which in turn cross-react with human neuronal gangliosides, resulting in neuropathy. After recovery, patients often have high levels of anti-ganglioside antibodies for over a decade.

However, these antibodies no longer cause neuropathy when tested using a human pluripotent stem cell-derived sensory neuron model with human complement. The study reveals differences in IgG subclass and glycoform between acute and recovered GBS patient sera, encompassing anti-inflammatory modifications on isolated anti-GM1 ganglioside antibodies.

The findings suggest that GBS patients develop non-pathogenic variants of autoantibodies that are unable to damage their neurons but may still offer protection against C. jejuni infection.