The relation of clinical disease to antibody titre, proliferative response and neurophysiology in murine experimental autoimmune myasthenia gravis.
Murine myasthenia is a relatively faithful model of the human disease. We studied anti-AChR antibody titres, lymphocyte proliferative response to AChR, characteristic electromyographic (EMG) abnormalities and muscle strength at weekly intervals after immunization of C57B16J mice with Torpedo AChR. The boosting immunization at 1 month after the primary immunization resulted in a progressive increase of anti-AChR IgG antibodies, but caused a marked drop in the proliferative response. Although characteristic EMG abnormalities occurred in nearly all immunized mice, clinical disease appeared very late or not at all. These data parallel findings in human myasthenia.
D000109:Acetylcholine; D000818:Animals; D000917:Antibody Formation; D001327:Autoimmune Diseases / Q000276:immunology; D004576:Electromyography; D004591:Electrophoresis, Polyacrylamide Gel; D005260:Female; D007074:Immunoglobulin G / Q000096:biosynthesis; D008213:Lymphocyte Activation; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009132:Muscles / Q000503:physiopathology; D009157:Myasthenia Gravis / Q000276:immunology* / Q000503:physiopathology; D011950:Receptors, Cholinergic / Q000276:immunology*; D013997:Time Factors
D007074:Immunoglobulin G; D011950:Receptors, Cholinergic; D000109:Acetylcholine