| AMA | 1) Anti-Mitochondrial Antibodies 2) American Medical Association |
|---|---|
| Anti-LKM | Antibodies to Liver-Kidney Microsome |
| FA | 1) Fatty Acid 2) Fluorescent Antibodies; Çü±¤ Ç×ü |
| MAbs | Monoclonal Antibodies |
| MHA-TP | Micro-Hemagglutination Assay for antibodies to Treponema Pallidum |
| AEA | A-anti-endomysium antibodies |
|---|---|
| ANCA | Anti-Neutrophil Cytoplasmic Antibodies |
| ACA | Anti-cardiolipin antibodies |
| ACL | Anti-cardiolipin antibodies |
| ACLA | Anti-cardiolipin antibodies |
| striational antibodies | <immunology> Thymoma occur in approximately 15% of patients with myasthenia gravis. Striational antibodies are found in 90% of patients with both myasthenia gravis and thymoma and are present in only 6% of myasthenia gravis patients <40 years of age without thymoma. They are absent in 82-100% of all patients with myasthenia gravis but without thymoma. The absence of striational antibodies argues against a thymoma in a patient with myasthenia gravis. Elevated values of striational antibodies (predominantly IgM) are found in 25% of patients with rheumatoid arthritis treated with penicillamine. They are also useful when monitoring immunosuppressive therapy for detection of autoimmune complications of bone marrow transplantation including graft-versus-host disease. Measurement of striational antibodies and acetylcholine receptor antibodies is useful for predicting risk of myasthenia gravis in patients with thymoma and for predicting recurrence of thymoma. Antibodies to titin, which comprise at least some of the striational antibodies which react with the I band near the A-1 junction, are highly associated with the presence of thymoma in myasthenia gravis. Alpha-smooth muscle (alpha-SM) is also associated with striational antibodies. The alpha-SM actin isoform is expressed normally by vascular SM cells and by stromal fibroblastic cells in pathological conditions leading to fibrosis. Upregulatation of alpha-SM actin in the glomerulus indicates mesangial cell activation and is not always correlated with the degree of glomerulosclerosis. The relatively high incidence for ASA (anti-smooth muscle antibody) suggests that immune-mediated processes might be involved in the etiology of sudden deafness. (16 Dec 1997) |
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| acetylcholine receptor antibodies | <neurology, investigation> A test used to measure the amount of antibodies to acetylcholine receptors on nerve endings. This is a diagnostic test for myasthenia gravis. A normal value is no antibodies in the bloodstream. Acetylcholine receptor (AChR) binding autoantibodies (i.e. Antibodies reactive with several epitopes other than the binding site for acetylcholine or alpha-bungarotoxin) are present in approximately 88% of patients with generalised myasthenia gravis, 70% of ocular myasthenia and in approximately 80% of myasthenia gravis in remission. Although serum concentrations of AChR binding autoantibodies do not in general correlate well with severity of weakness, there is typical decrease in concentration as weakness improves with immunosuppressive therapy. AChR blocking autoantibodies (i.e., antibodies reactive with the AChR binding site) are present in about 50% of patients with myasthenia gravis, 30% with ocular myasthenia gravis and 20% of myasthenia gravis in remission, AChR blocking autoantibodies are the only AChR autoantibodies present in about 1% of myasthenia gravis. AChR modulating autoantibodies (i.e., autoantibodies which cross-link AChRs and cause their removal from muscle membrane surfaces) are present in more than 90% of myasthenia gravis and occasionally are the only AchR autoantibodies detectable in mild, recent onset or ocular-restricted myasthenia gravis. Results for AChR modulating autoantibodies can be transiently false-positive due to curare-like drugs used during general anesthesia. AChR autoantibodies of one or more types are found in at least 80% of ocular myasthenia gravis. Although generally absent in neurological conditions other than myasthenia gravis(and consequently unlikely to cause confusion in neurodiagnosis), false-positive results for AChR autoantibodies occasionally occur in primary biliary cirrhosis, tardive dyskinesia, autoimmune thyroiditis, the elderly, amyotrophic lateral sclerosis patients treated with cobra venom and patients with thymoma in the absence of myasthenia gravis. Approximately 1% of patients with rheumatoid arthritis treated with D-penicillamine develop AChR autoantibodies and myasthenia gravis, both of which disappear when the drug is discontinued. Babies born to ~10% of myasthenia gravis mothers have a transient neonatal form of myasthenia gravis that responds well to anticholinesterase therapy and usually remits within 1 month as maternal IgG disappears. (29 Dec 1997) |
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| antibodies | Any of numerous protein molecules produced by the B-cells as a primary immune defense. (16 Dec 1997) |
| antibodies, anticardiolipin | Antiphospholipid antibodies found in association with systemic lupus erythematosus (lupus erythematosus, systemic), antiphospholipid syndrome, and in a variety of other diseases as well as in healthy individuals. The antibodies are detected by solid-phase immunoassay employing the purified phospholipid antigen cardiolipin. (12 Dec 1998) |
| antibodies, anti-idiotypic | Antibodies which react with the individual structural determinants (idiotopes) on the variable region of other antibodies. (12 Dec 1998) |
| antibodies, antineutrophil cytoplasmic | Autoantibodies directed against cytoplasmic constituents of polymorphonuclear leukocytes and/or monocytes. They are used as specific markers for wegener's granulomatosis and other diseases, though their pathophysiological role is not clear. Anca are routinely detected by indirect immunofluorescence with three different patterns: c-anca (cytoplasmic), p-anca (perinuclear), and atypical anca. (12 Dec 1998) |
| antibodies, antinuclear | See: Antinuclear antibodies. (12 Dec 1998) |
| antibodies, antiphospholipid | Autoantibodies directed against phospholipids. These antibodies are characteristically found in patients with systemic lupus erythematosus (lupus erythematosus, systemic), antiphospholipid syndrome, related autoimmune diseases, some non-autoimmune diseases, and also in healthy individuals. (12 Dec 1998) |
| antibodies, archaeal | Immunoglobulins induced by substances elaborated by archaea that have an antigenic activity. (12 Dec 1998) |
| antibodies, bacterial | Immunoglobulins induced by substances elaborated by bacteria that have an antigenic activity. (12 Dec 1998) |
| antibodies, bispecific | Antibodies, often monoclonal, in which the two antigen-binding sites are specific for separate antigenic determinants. They are artificial antibodies produced by chemical crosslinking, fusion of hybridoma cells, or by molecular genetic techniques. They function as the main mediators of targeted cellular cytotoxicity and have been shown to be efficient in the targeting of drugs, toxins, radiolabelled haptens, and effector cells to diseased tissue, primarily tumours. (12 Dec 1998) |
| antibodies, blocking | Antibodies that inhibit the reaction between antigen and other antibodies or sensitised T-lymphocytes (e.g., antibodies of the IgG class that compete with IgE antibodies for antigen, thereby blocking an allergic response). Blocking antibodies that bind tumours and prevent destruction of tumour cells by cytotoxic T-lymphocytes have also been called enhancing antibodies. (12 Dec 1998) |
| antibodies, catalytic | Antibodies that can catalyze a wide variety of chemical reactions. They are characterised by high substrate specificity and share many mechanistic features with enzymes. (12 Dec 1998) |
| antibodies, fungal | Immunoglobulins induced by substances elaborated by fungi that have an antigenic activity. (12 Dec 1998) |
| antibodies, helminth | Antibodies produced by human or animal cells following clinical or experimental exposure to parasitic helminth antigens. The IgE class of immunoglobulins is usually formed and released, but IgG, IgM, and IgA may also occur. (12 Dec 1998) |
| antibodies, heterophile | Antibodies elicited in a different species from which the antigen originated. These antibodies are directed against a wide variety of interspecies-specific antigens, the best known of which are forssman, hanganutziu-deicher (h-d), and paul-bunnell (p-b). Incidence of antibodies to these antigens--i.e., the phenomenon of heterophile antibody response--is useful in the serodiagnosis, pathogenesis, and prognosis of infection and latent infectious states as well as in cancer classification. (12 Dec 1998) |
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