Eye Muscle Antibodies in Patients with Ocular Myasthenia Gravis: Possible Mechanism for Eye Muscle Inflammation in Acetylcholine-Receptor Antibody-Negative Patients

摘要: Myasthenia gravis is an organ-specific autoimmune disorder generally thought to be caused by antibody-mediated attack against the skeletal muscle nicotinic acetylcholine (Ach) receptor (AchR) at neuromuscular junction. Extraocular weakness and double vision are present in about 90% of patients with myasthenia predominant complaints 20% patients, when condition called ocular (OMG). While serum antibodies AchR detected most generalized (GMG), they not found one-third variety, epidemiological, clinical, serological studies suggest that OMG GMG two separate diseases. Both forms sometimes associated thyroid autoimmunity or thyroid-associated ophthalmopathy (TAO). We have therefore tested sera Western blotting for porcine eye membrane proteins general, enzyme-linked immunosorbent assays (ELISA) specifically reaction antigens which prominent marker TAO, namely, calcium-binding protein calsequestrin so-called "64-kDa protein." The 64-kDa has recently been identified as flavoprotein subunit mitochondrial succinate dehydrogenase. Patients were excluded. Nine had Graves' hyperthyroidism without evident one Hashimoto's thyroiditis. Antibodies M(r) 15-110 kDa OMG, more being 100% 88% those OMG. frequently targeting 15, 67, 110 kDa. reactive purified (63 kDa) 21% but no patient GMG. recognizing dehydrogenase (67 42% (5 5) GMG, 48% all hyperthyroidism. There was close correlation between any muscle-reactive antibody either group myasthenic patients. findings support notion immunoreactivity other than may play a role development antibody-negative although it unlikely demonstrated this study directly implicated. Similarly, while demonstration TAO raises possibility link lesions disease common antigen(s), likely both disorders mediated cytotoxic T cells another cell antigen, such novel shared G2s, Fp markers immune-mediated reaction.