2002
DOI: 10.1016/s0022-510x(02)00200-9
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The role of antibodies in myasthenia gravis

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Cited by 39 publications
(23 citation statements)
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“…In line with this notion, patients who develop myasthenia gravis have circulating 150 kDa autoantibodies that reach the neuromuscular junction, bind to the acetylcholine receptor, and block cholinergic transmission. [45][46][47] Finally, our experiments demonstrated that WZ1-14.2.1 may function in physiologic conditions (pH 7.4, 37 °C) we reproduced in the modified Ellmann assay. On the other hand, the mass/activity ratio (i.e., the specific activity of WZ1-14.2.1) is probably inappropriate for its clinical use, due to the need of administering the active principle in the order of grams/dose, been the abzyme more than one-thousand weaker in terms of k cat than acetylcholinesterase.…”
Section: Discussionsupporting
confidence: 51%
“…In line with this notion, patients who develop myasthenia gravis have circulating 150 kDa autoantibodies that reach the neuromuscular junction, bind to the acetylcholine receptor, and block cholinergic transmission. [45][46][47] Finally, our experiments demonstrated that WZ1-14.2.1 may function in physiologic conditions (pH 7.4, 37 °C) we reproduced in the modified Ellmann assay. On the other hand, the mass/activity ratio (i.e., the specific activity of WZ1-14.2.1) is probably inappropriate for its clinical use, due to the need of administering the active principle in the order of grams/dose, been the abzyme more than one-thousand weaker in terms of k cat than acetylcholinesterase.…”
Section: Discussionsupporting
confidence: 51%
“…We note that with the exception of anti-DNA antibodies in systemic lupus erythematosus, 36 there are no well-defined relationships between antibody titers and disease activity. In fact, this is not even the case for antibody-mediated diseases such as myasthenia gravis 37 or idiopathic Addison disease. 38 Our analysis of serum anti-NPC demonstrates that patients who are anti-NPC-positive at the time of initial assessment tend to manifest consistent serum titers over time, thus indicating that anti-NPC are stable; on the other hand, we also found that patients who are initially anti-NPC-negative can subsequently become anti-NPC-positive.…”
Section: Discussionmentioning
confidence: 99%
“…Auto-antibodies directed against the α-subunit of the AChR on the postsynaptic membrane of the neuromuscular junction are thought to be the main cause of neuromuscular transmission failure in MG, resulting in skeletal muscle fatigue and weakness (De Baets and Stassen, 2002). From this point of view, one of the therapeutic approaches often used for autoimmune MG includes immunosuppressive therapy.…”
Section: Discussionmentioning
confidence: 99%