Disease relevance of Myasthenia Gravis

• To determine the potential importance of an immune response directed against the acetylcholine receptor in myasthenia gravis, we studied cell-mediated immunity to receptor as measured by lymphocyte stimulation in 21 myasthenic patients and 21 controls, including five with amyotrophic lateral sclerosis [1].
• We performed the same studies in eight patients with myasthenia gravis who were receiving cyclosporine and eight who were not, in five patients with essential hypertension, and in nine normal controls [2].
• We randomly assigned 20 patients with progressively worsening generalized myasthenia gravis of recent onset whose illness was not controlled by anticholinesterase therapy to treatment with either cyclosporine (6 mg per kilogram of body weight per day) or placebo [3].
• Sharing of antigenic determinants between the nicotinic acetylcholine receptor and proteins in Escherichia coli, Proteus vulgaris, and Klebsiella pneumoniae. Possible role in the pathogenesis of myasthenia gravis [4].
• Pyridostigmine, a carbamate acetylcholinesterase (AChE) inhibitor, is routinely employed in the treatment of the autoimmune disease myasthenia gravis [5].

Psychiatry related information on Myasthenia Gravis

• These A2 receptor-mediated adenosine actions might have potential therapeutic interest, in particular in movement disorders such as Parkinson's disease and Huntington's chorea, as well as in schizophrenia, Alzheimer's disease, myasthenia gravis and myasthenic syndromes [6].
• This pyridine derivative has also been shown to inhibit T cell proliferation, to modulate immune responses and to alleviate some of the symptoms associated with neurological disorders such as multiple sclerosis, myasthenia gravis and Alzheimer's disease [7].

High impact information on Myasthenia Gravis

• Immunology of acetylcholine receptors in relation to myasthenia gravis [8].
• Myasthenia gravis unmasked by cocaine abuse [9].
• In both the patients who were studied electromyographically, pretreatment and postplacebo responses were typical of myasthenia gravis and became normal after edrophonium [10].
• Thymosin alpha 1 in myasthenia gravis [11].
• Plasmapheresis combined with prednisone and azathioprine therapy produced striking clinical improvement in five patients with myasthenia gravis who still had moderate to severe disability despite thymectomy, high-dose prednisone therapy and optimal doses of cholinesterase inhibitors [12].

Chemical compound and disease context of Myasthenia Gravis

• Cyclosporine for myasthenia gravis [13].
• Auto-antibodies to the receptor tyrosine kinase MuSK in patients with myasthenia gravis without acetylcholine receptor antibodies [14].
• Electrophysiological and pharmacological changes typical of myasthenia gravis were recorded, including decremental responses to repetitive stimuli, curare sensitivity, neostigmine reversal, and posttetanic phenomena [15].
• Daily injections into mice of an ammonium sulfate-precipitated immunoglobulin fraction of serum from patients with myasthenia gravis were carried out for up to 14 days [16].
• A 59-year-old woman with myasthenia gravis who received a large dose of pyridostigmine bromide developed postoperative psychosis and was diagnosed as having bromide intoxication [17].

Biological context of Myasthenia Gravis

• Our findings are further evidence that autoimmunity to the acetylcholine receptor plays a central part in myasthenia gravis [1].
• Cellular immunity in myasthenia gravis. Response to purified acetylcholine receptor and autologous thymocytes [1].
• Maternal-fetal transmission of myasthenia gravis with acetylcholine-receptor antibody [18].
• Regulation of acetylcholine receptor gene expression in human myasthenia gravis muscles. Evidences for a compensatory mechanism triggered by receptor loss [19].
• Humoral immunity in myasthenia gravis: relationship to disease severity and steroid treatment [20].

Anatomical context of Myasthenia Gravis

• The pathogenesis of myasthenia gravis involves a humorally mediated autoimmune attack directed against acetylcholine receptors of skeletal muscles [21].
• Accelerated degradation of acetylcholine receptors at neuromuscular junctions may represent an important antibody-mediated mechanisms in myasthenia gravis [22].
• Autoimmune T lymphocytes in myasthenia gravis. Determination of target epitopes using T lines and recombinant products of the mouse nicotinic acetylcholine receptor gene [23].
• Cathepsin V is involved in the degradation of invariant chain in human thymus and is overexpressed in myasthenia gravis [24].
• T helper cell recognition of muscle acetylcholine receptor in myasthenia gravis. Epitopes on the gamma and delta subunits [25].

Gene context of Myasthenia Gravis

• Numbers of cells responding to AChR in MS and MBP in myasthenia gravis did not differ from numbers found in absence of antigen [26].
• In myasthenia gravis (MG), TNF and IL-1beta polymorphisms and high serum levels of these proinflammatory cytokines have been observed [27].
• Mice with IFN-gamma receptor deficiency are less susceptible to experimental autoimmune myasthenia gravis [28].
• Overexpression of IFN-induced protein 10 and its receptor CXCR3 in myasthenia gravis [29].
• HLA-DPB1 allele associates with early-onset myasthenia gravis in Japan [30].

Analytical, diagnostic and therapeutic context of Myasthenia Gravis

• Our results suggest that plasmapheresis will find a place in the management of patients with myasthenia gravis, and they implicate antibodies to acetylcholine receptor as a pathogenic factor in this disease [12].
• Autoimmune response to acetylcholine receptors in myasthenia gravis and its animal model [31].
• These data provide further support for the view that myasthenia gravis is a consequence of thymic disease associated with systemic release of thymopoietin, with ensuing neuromuscular block [32].
• Immunosuppression of experimental autoimmune myasthenia gravis by azathioprine. II. Evaluation of immunological mechanism [33].
• Thymoma-associated myasthenia gravis. Transplantation of thymoma and extrathymomal thymic tissue into SCID mice [34].

References