We have investigated the hypothesis that the pathogenesis of Guillain-Barré syndrome (GBS) involves an autoimmune T cell response to P0 and P2 proteins of peripheral nerve myelin. The proliferative responses of blood mononuclear cells (MNC) to myelin proteins and synthetic peptides derived from them were determined in patients with GBS and chronic idiopathic demyelinating polyradiculoneuropathy (CIDP), normal controls (NC) and patients with other neuropathies (ONP). Twelve out of 19 GBS patients responded to P0 or P2, 6 to P0 and its peptides only, 3 to P2 and its peptides only, and 3 to both P0 and P2 antigens. Responses to at least one of the antigens were also found in 6/13 of CIDP patients, but in only 4/17 NC and 2/6 ONP. Immune responses in GBS are heterogeneous. The early T cell responses to P0 protein, described here for the first time, may be important in the pathogenesis of some cases.