David Andersson will review studies which demonstrate that fibromyalgia is an autoantibody mediated condition. These recent investigations have shown that sensory, motor, and anatomical symptoms and signs of fibromyalgia can be transferred to mice by administration of IgG from patients. In mice, patient IgG produces behavioral sensory hypersensitivities that are accompanied by functional abnormalities in peripheral nociceptive afferent nerve fibers.  Hypersensitivities produced by fibromyalgia IgG in mice are reversible and typically resolve within 2–3 weeks, suggesting that reduction of IgG may be an effective therapeutic rationale.  He will further present electrophysiological investigations of single units in skin-nerve preparations and of neurons isolated from mice treated with IgG from patients or healthy control subjects. The results suggest that sensitization of sensory afferents may explain both painful hypersensitivities and other sensory abnormalities reported by fibromyalgia patients.