重症筋無力症のリンパ球からみた病因病態論

Progress in research of the cellular immunity for the pathogenesis of myasthenia gravis.

　重症筋無力症（myasthenia gravis, MG）が自己免疫疾患であることはほぼ明らかであるとすると，病因の解明のためには，自己免疫つまり自己寛容の破綻に対する免疫学的機序を明らかにしなければならない。

　免疫学の進歩により，自己寛容成立の機序が明らかになっていくとともに，MGの病因も徐々にその本質が解明されると考えられる。ヒトMGのモデル動物と考えられるEAMG（experimental allergic myastheniagravis）のマウスでの作製およびその成立機序の解明は，ヒトMGの病因の解明に寄与することが大きいと考えられる。

Myasthenia gravis (MG) is a disease caused by a defect in a neuromuscular transmission of acetylcholine. It has been suggested that MG is one of autoimmune diseases since acetylcholine receptor (AChR) antibodies are detected in the sera of myasthenic patients. The experimental model of MG was induced in animals by the immunization with AChR purified from Torpedo narke (experimental allergic myasthenia gravis, EAMG). It is a useful model to clarify the regulatory mechanism of anti-AChR-antibody production by T cells and the gene locus controlling the immune response to AChR antigen.It was shown that AChR-specific helper or sup-pressor T cells were induced in the mice with EAMG and these cells secreted AChR specific factor that mediated helper or suppressive effect. The gene locus controlling the immune response to AChR will be determined through the analysis of these factors.