REACTIVITY OF T-CELLS FROM SERONEGATIVE PATIENTS WITH MYASTHENIA-GRAVIS TO T-CELL EPITOPES OF THE HUMAN ACETYLCHOLINE-RECEPTOR

Seronegative (SN) patients with myasthenia gravis (MG) have clinical a nd electrophysiologic features similar to those of seropositive (SP) p atients, and they respond to the same therapeutic measures. However, b ecause SN patients lack detectable (by standard radioimmunoassays) ser um antibodies to acetylcholine receptor (AChR), which are considered t o have a crucial role in MG, the pathophysiologic basis for the diseas e is not clear. We therefore compared the ability of peripheral blood lymphocytes (PBL) of SN patients (11) and SP patients (39) to respond to myasthenogenic T cell epitopes of human AChR. We tested two aspects that relate to T-cell immunity: 1) T cell responses to myasthenogenic peptides by proliferation and IL-2 production, and 2) the ability of antigen-presenting cells to bind these T-cell epitopes. T cells of SN patients did not differ from those of SP patients in their ability to respond and to bind the two human AChR-derived myasthenogenic peptides . This supports the belief that most SN patients indeed suffer from an autoimmune disease directed against the AChR. The presence of T-cell immunity in the absence of antibodies may emphasize the importance of AChR specific T cells in MG.