CD19 and Guillain-Barre syndrome: Evidence in favor of involvement of humoral immunity in the pathogenesis of GBS include studies that have reported deposition of immunoglobulin G and complement activation products on the axolemma of motor fibers11; and the presence of myelin specific plasmablasts and B cell expansion in spontaneous autoimmune polyneuropathy (SAP), an animal model of GBS, and depletion of these cells in response to anti-CD19 monoclonal antibody (mAb) treatment, leading to attenuation of disease severity12.