Studies on the nature of autoimmunity in myasthenia gravis. Evidence for an immunodeficiency type.
Clinical and laboratory data continue to support the concept of a genetically determined breakdown of immunological tolerance in myasthenia gravis with immunological damage to the motor end plates. The demonstration of impaired function of thymus-derived lymphocytes and of IgA deficiency correlate well with the clinical data in which there is an increase incidence of autoimmune diseases associated with anergy. Whilst the exact pathogenesis of myasthenia gravis is unknown, the available data support the concept of an immune deficiency disorder.
D000917:Antibody Formation; D000937:Antigen-Antibody Reactions; D001327:Autoimmune Diseases / Q000276:immunology*; D003165:Complement System Proteins / Q000378:metabolism; D005796:Genes; D006680:HLA Antigens; D006801:Humans; D007108:Immune Tolerance; D007111:Immunity, Cellular; D007136:Immunoglobulins / Q000378:metabolism; D007153:Immunologic Deficiency Syndromes / Q000276:immunology*; D037102:Lectins / Q000494:pharmacology; D008213:Lymphocyte Activation; D007959:Lymphocyte Culture Test, Mixed; D009157:Myasthenia Gravis / Q000235:genetics / Q000276:immunology*; D014176:Protein Biosynthesis; D013601:T-Lymphocytes / Q000276:immunology; D013934:Thymectomy
D006680:HLA Antigens; D007136:Immunoglobulins; D037102:Lectins; D003165:Complement System Proteins