Antibodies to neurofascin exacerbate adoptive transfer experimental autoimmune neuritis

- Neurofascin antibodies are found in the sera of some patients with GBS or CIDP.
- Antibodies to neurofascin exacerbate experimental autoimmune neuritis.
- Antibodies to neurofascin cause conduction defects when injected intraneurally.

Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathy are autoimmune disorders of the peripheral nervous system in which autoantibodies are implicated in the disease pathogenesis. Recent work has focused on the nodal regions of the myelinated axon as potential autoantibody targets. Here we screened patient sera for autoantibodies to neurofascin and assessed the pathophysiological relevance of anti-neurofascin antibodies in vivo. Levels of anti-neurofascin antibodies were higher in sera from patients with Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathy when compared with those of controls. Anti-neurofascin antibodies exacerbated and prolonged adoptive transfer experimental autoimmune neuritis and caused conduction defects when injected intraneurally.