Yozo Shimizu

SURFACE ULTRASTRUCTURE AND MICROVISCOSITY OF LYMPHOCYTE MEMBRANES IN MYASTHENIA GRAVIS

Myasthenia gravis (MG) is a disease caused by the impairment of neuromuscular junctions and characterized by high incidence of thymic involvement including thymoma or thymic hyperp1asia.l It has been demonstrated that the antibody against acetylcholine receptors (AChR) is present in sera of MG patienh2 The AChR has been found not only in synaptic membranes but also in thymic epithelial cells and thymic lymphocyte^.^ The antibody against AChR (anti-AChR antibody) is responsible for abnormality of neuromuscular j ~ n c t i o n . ~ Although direct evidence that peripheral lymphocytes of MG patients bear AChR is not found at present, abnormal findings such as decreased mitogenic activities,G higher response to AChR,7 and decreased T-cell in MG lymphocytes, and B-cell clone in the thymus were revealed. This evidence indicated that cell-mediated immune responses represented by lymphocytes play significant roles in the pathogenesis of MG. It is, therefore, of great interest to study the surface structures and functions of myasthenic lymphocytes resulting from the interaction between their receptors and anti-receptor antibodies since the impaired postsynaptic membrane is caused by the analogous interaction between AChR and the anti-AChR antibodies. The morphological alteration of cell surface can be observed by radioautography, ferritin or enzyme conjugated immunoelectron microscopy, immunoscanning electron microscopy and freeze-fractured technique. The functional changes in cell membranes can be evaluated by measuring the receptor activities and membrane microviscosity.8 We studied the relation between ultrastructural alterations and microviscosity of the cell membrane in the peripheral blood lymphocytes from MG patients, from the viewpoint that the alteration of MG lymphocyte membranes may represent the impairment of postsynaptic membranes in MG.