Recovery from Guillain-Barré syndrome is associated with increased levels of neutralizing autoantibodies to interferon-gamma

Abstract

Guillain-Barré syndrome (GBS) is an immune-mediated demyelinating disease of peripheral nerves that is often preceded by an infection and is usually self-restricted. The Th1 cytokine interferon-gamma (IFN-gamma) is thought to be disease-promoting in organ-specific autoimmune diseases. We report the spontaneous induction of IFN-gamma and a mechanism involving the generation of neutralizing autoantibodies (Aabs) to IFN-gamma that may regulate the disease. Numbers of cells spontaneously secreting IFN-gamma in peripheral blood were augmented in GBS, in particular at the peak of clinical disease, and decreased during recovery. This decrease was associated with elevated serum concentrations of IgG Aabs to IFN-gamma. These Aabs specifically bound to IFN-gamma and neutralized its effects in a biological assay. Aabs to IFN-gamma are proposed to be another important regulatory mechanism in IFN-gamma-driven GBS.