Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004364 (autoimmune disease)
 24,845 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The infusion of high-dose (275 mg/kg body weight) immune globulin intravenous (IGIV) after 466 plasma exchanges in 64 patients with autoimmune disease was studied. Side effects occurred during 15% of IGIV infusions. For the most part they were transient and mild, and could be controlled by slowing the infusion rate. Two percent of infusions had to be terminated because of more persistent or severe side effects. Chills were the most common side effect, followed by nausea, flushing, anxiety, and nausea. Serum IgG levels were immediately restored into the normal range by IGIV infusions, and they were much more effective in restoring IgG levels after plasma exchange than intramuscular injection of 9.9 g of immune serum globulin (ISG). Up to 15 weekly high-dose IGIV infusions were well tolerated without unusual side effects. These patients did not have any major bacterial infections, but were not protected from developing Herpes zoster at the dosages used. In patients with myasthenia gravis, a short term impact of a single IGIV infusion on titers of antibody to acetylcholine receptor could not be demonstrated. This study showed IGIV to be a safe and effective preparation for the replacement of normal IgG removed during plasma exchange.
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PMID:Immune globulin intravenous replacement after plasma exchange. 668 80

Electrolectin (EL), an endogenous beta-D-galactoside-binding lectin from Electrophorus electricus, was found to have a prophylactic and therapeutic action on the experimental autoimmune myasthenia gravis (EAMG) in rabbits. EAMG is an autoimmune disease induced by immunization with the purified acetylcholine receptor protein (AChR) and is considered to be a good model for the human disease myasthenia gravis. Simultaneous immunization with AChR and EL completely prevented the onset of myasthenic symptoms. This preventive effect was accompanied by a decrease in the recognition of AChR by anti-AChR antibodies. The administration of EL to myasthenic rabbits led, in most cases, to a complete recovery which was not accompanied by any significant change in the level of circulating anti-AChR antibodies. No evidence for an action of EL at the muscular level could be obtained. EL, however, was found to bind to rabbit lymphocytes and to stimulate their mitosis. These results suggest that EL produces its effects on EAMG by acting at the level of the immune system. It is proposed that EL may play a role in the immunological regulation of the response to self-antigen, which could be one of the biological functions of this animal lectin.
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PMID:Prevention and therapy with electrolectin of experimental autoimmune myasthenia gravis in rabbits. 686 75

Autoimmune diseases, including myasthenia gravis, occur in patients treated with D-penicillamine. Because D-penicillamine might induce autoantibodies by the mechanism of antigenic alteration, we studied the reaction of D-penicillamine with purified acetylcholine receptor from Torpedo californica. We found that brief exposure to D-penicillamine resulted in its covalent attachment to two receptor subunits, alpha (40,000 daltons) and gamma (59,000 daltons), presumably by reduction and formation of mixed disulfides. Furthermore, D-penicillamine treatment resulted in a dramatic modification of the equilibrium acetylcholine binding properties of both purified receptor and receptor-rich membrane fragments.
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PMID:Penicillamine-induced myasthenia gravis: effects of penicillamine on acetylcholine receptor. 688 94

We have treated animals with an ongoing autoimmune disease, experimental autoimmune myasthenia gravis (EAMG), using a strategy designed to eliminate the antibody-producing cells. During well-established EAMG, a single high dose of cyclophosphamide was given because of its known effectiveness against B-lymphocytes. To counteract the lethal effects of the drug, the rats were "rescued" by bone marrow cell transplantation. This treatment produced a rapid and sustained fall of antibody titers against both the immunizing antigen (Torpedo acetylcholine receptor) and the autoantigen (rat acetylcholine receptor). Immunologic memory, as measured by an anamnestic response to the antigen, was partially suppressed. Cyclophosphamide treatment produced improvement in the neuromuscular defect: treated animals had, on the average, twice as many acetylcholine receptors at neuromuscular junctions compared with untreated EAMG animals. This treatment method of short-term high doses of an immunosuppressive drug, such as cyclophosphamide, may eventually prove useful for human myasthenia gravis and other autoimmune diseases.
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PMID:Treatment of ongoing experimental myasthenia gravis with short term high dose cyclophosphamide. 697 88

Myasthenia gravis is characterized by muscle weakness, which is alleviated by rest and by anticholinesterase drugs. There are two forms of the disease in the dog, acquired and congenital. The acquired form occurs either in young adults, or in older animals that have developed mediastinal tumors. Clinically, there is weakness of the muscles of the limbs, neck, and head, together with dilatation of the esophagus. In some cases, circulating antibody to acetylcholine receptor is present and the amount of receptor in the end-plates is decreased. It is thought to be an autoimmune disease. The congenital form of canine myasthenia gravis occurs most frequently in Jack Russell terriers from six to eight weeks of age. The clinical manifestations are similar to those accompanying acquired myasthenia, although dilatation of the esophagus is not a feature. Raised antibody levels to acetylcholine receptor have not been noted, although the amount of receptor in the end-plates is decreased. Thus, the congenital form does not appear to be an autoimmune disease and the pathophysiology has yet to be established. Both forms of canine myasthenia gravis provide useful models analogous to the disease in man.
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PMID:Myasthenia gravis. 699 86

Symptoms of myasthenia gravis in infancy may occur from passive transfer of maternal disease, acquired autoimmune disease, or nonautoimmune hereditary disease. Of nine patients with infantile-onset myasthenia who were not born to mothers with the disease, two had detectable antibody to acetylcholine receptor. Patients with or without antibodies were clinically indistinguishable, except for the occurrence of similar disease in siblings of patients without antibody. Differentiation of autoimmune and hereditary, myasthenia in infancy is necessary for appropriate therapeutic measures and genetic counseling. Antibody determinations provide a useful aid in this differentiation.
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PMID:Myasthenia gravis in infancy. 719 42

Myasthenia gravis (MG) is a disease which occurs as a consequence of an autoimmune response directed against the nicotinic acetylcholine receptor (AChR) of the myoneural junction. Antisera raised against complex antigens such as AChR comprise a mixture of antibodies reactive with various determinants on the antigen molecule. The antibodies against any single determinant may be of several immunoglobulin classes and idiotypes. Antibodies produced by cloned lymphocyte-myeloma hybridoma cell lines have provided a way of analysing the diverse components making up a polyclonal antiserum and assessing the relative contribution made by each to the overall immune reaction in vivo. We have applied this technique to the investigation of the autoimmune response in MG. We demonstrate here that certain monoclonal anti-Torpedo AChR antibodies, when injected intravenously into normal rats, induce an acute myasthenic syndrome. Thus binding of a single molecular species of antibody reactive with a single antigenic determinant can result in all of the manifestations of an autoimmune disease.
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PMID:Monoclonal anti-acetylcholine receptor antibodies can cause experimental myasthenia. 741 61

Myasthenia Gravis (MG) is an autoimmune disorder which compromises neuromuscular transmission. The hallmark of the disorder is fatigue with repetitive activity. Patients may experience symptoms ranging from double vision, ptosis and weak voice to choking, shortness of breath, generalized weakness and respiratory failure. The clinical diagnosis is confirmed by identification of a decremental response to repetitive nerve stimulation by electromyography (EMG), the presence of serum antibodies to the muscle acetylcholine receptor (AChR), or an improvement in strength with administration of intravenous edrophonium. With improvements in critical care and immunosuppressive treatments, MG is rarely the grave disease it once was, but because of the odd fatiguing symptoms and relative rarity of the disorder, patients are frequently misdiagnosed and their special needs overlooked. The nature of MG, with its acute and chronic components, creates complex needs for affected individuals and their families. The advanced practice nurse in collaboration with a neurologist in the outpatient setting is positioned to address these needs in an ongoing case management role.
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PMID:Myasthenia gravis: pathophysiology, diagnosis and collaborative care. 749 22

The autoimmune disease myasthenia gravis (MG), caused by the effect of specific antibodies, directed towards the nicotinic acetylcholine receptor, is triggered by autoantigen-specific T cells. In order to investigate cellular parts of the immune response in MG, the authors investigated the binding of the nicotinic acetylcholine receptor (AChR) to peripheral blood mononuclear cells (PBMC) from MG patients. AChR binding cells were identified by rosetting experiments using AChR-coated fluorescein beads. Applying this technique, a significant percentage of PBMC (21.2 +/- 7.65%) from MG patients formed rosettes with AChR-coated beads. Membrane preparations of nycodenz- or percoll-separated monocytes from MG patients or T-cell depleted monocytic subpopulations were applied to SDS-PAGE under reducing conditions. Ligand-blotting studies with biotinylated AChRs revealed two cell-membrane proteins with molecular weights of 58- and 78-kD. In parallel the same results were obtained by affinity chromatography of monocytic membrane proteins using AChR-sepharose. A possible interference of anti-AChR IgG was excluded. The 58- and the 78-kD proteins are detectable under reducing conditions by ligand blotting with AChR-biotin, while under non-reducing conditions only the 58-kD protein can be detected. Furthermore, in experiments using Endoglycosidase-H, the 58-kD protein appears to be non-glycosylated, while the 78-kD protein bears carbohydrates. These findings suggest that monocytes which bind the AChR via specific membrane proteins on their surface might act as antigen-presenting cells and may lead to an induction of the T-cell response, in the early phase of the disease.
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PMID:Characterization of a 58- and a 78-kD monocytic membrane protein with affinity to the acetylcholine receptor in myasthenia gravis patients. 751 Apr 15

In autoimmune disorders, inactivation of pathogenic antigen-specific T cells, rather than global immunosuppression, would be highly desirable. One way to achieve this would be to deliver the first antigen-specific signal to the T cell in the absence of the second costimulatory signal. Myasthenia gravis (MG) is a well-characterized autoimmune disease in which T cell-dependent autoantibodies are directed against the acetylcholine receptor (A ChR) at the neuromuscular junction. AChR-specific T cells have been cloned from MG patients, and in this study, we have induced long-lasting tolerance in vitro in one particular clone (PM-A1) with a known peptide epitope (alpha 144-163) and MHC class II restriction (DR4 Dw14.2 or 4.2) by using soluble MHC-class II peptide complexes. Preincubation of PM-A1 T cells with such complexes induced death by apoptosis in < or = 40-50% of the AChR-specific cells. Surviving cells remained refractory to stimulation with AChR-derived synthetic peptides or recombinant polypeptides for < or = 38 d after complex treatment. These effects were highly specific, dose-dependent and required > 2 h preincubation. The T cells could be protected from the tolerizing effects of complex by coincubation with DR-matched or -mismatched antigen-presenting cells. This work shows that antigen-specific T cells can be selectively killed or anergized using soluble MHC class II: peptide complexes. Such an antigen-specific therapy offers a rational approach to the immunotherapy of autoimmune or allergic disease in vivo.
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PMID:Specific tolerance to an acetylcholine receptor epitope induced in vitro in myasthenia gravis CD4+ lymphocytes by soluble major histocompatibility complex class II-peptide complexes. 751 79


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