Okadaic acid-like toxin in systemic lupus erythematosus patients: Hypothesis for toxin-induced pathology, immune dysregulation, and transactivation of herpesviruses
Identifieur interne : 002990 ( Main/Exploration ); précédent : 002989; suivant : 002991Okadaic acid-like toxin in systemic lupus erythematosus patients: Hypothesis for toxin-induced pathology, immune dysregulation, and transactivation of herpesviruses
Auteurs : T. M. Mitchell [États-Unis]Source :
- Medical Hypotheses [ 0306-9877 ] ; 1996.
English descriptors
- Teeft :
- Acad, Acetylcholine release, Antibody formation, Arthr rheum, Biochem biophys, Biol, Biol chem, Catecholamine secretion, Cell activation, Cell biol, Cell function, Cell membranes, Channel blocker, Clin, Clin immunol, Disease activity, Erythematosus, Frog lens, Herpes, Herpes simplex virus, Herpesviruses, Immune, Immune dysregulation, Immunol, Immunoregulatory subsets, Inhibitory activity, Interleukin, Kinase, Kinase activity, Long terminal, Lupus, Lupus erythematosus, Lymphocyte, Marine toxin, Marine toxins, Medical hypotheses, Memory phenotype, Okadaic, Okadaic acid, Okadaic toxin, Other diseases, Pathway, Patients exhibit, Persistent viruses, Phenotype, Phosphatase, Phosphatase inhibition, Phosphatase inhibitor, Phosphorylation, Preliminary experiment, Proc nail acad, Proc natl acad, Promoter, Protein phosphatases, Protein phosphorylation, Protein tyrosine kinase, Recent advances, Receptor, Repressive activity, Retinoblastoma gene product, Rheum, Rheumatoid arthritis, Serine, Signal transduction, Simplex, Sodium channels, Soluble receptor, Soluble receptors, Specific abnormalities, Systemic, Systemic lupus erythematosus, Systemic lupus erythematosus patients, Target cells, Toxin, Tumor necrosis factor, Tyrosine, Tyrosine phosphatase, Viral, Viral protein, Viral proteins, Virol.
Abstract
Abstract: Preliminary evidence suggests there is a toxin in the sera of systemic lupus erythematosus patients which reacts with a commercial enzyme-linked immunosorbent assay kit for the detection of the marine toxin, okadaic acid. Data is presented which supports the hypothesis that an okadaic acid-like toxin may be the principle agent of lymphocyte dysregulation in systemic lupus erythematosus and other immune-dysreguaated states. The okadaic acid-like toxin can produce the specific abnormalities in T-lymphocyte phenotype and function typical of systemic lupus erythematosus, principally through its ability to inhibit serine/threonine phosphatases necessary for secondary signalling processes, and through its ability to inhibit calcium which is crucial to protein kinase C-mediated signalling of T-lymphocytes. The disruption probably occurs through the protein tyrosine kinase p56lck pathway crucial for IL-2. Additionally, the toxin's ability to disrupt voltage-sensitive ion channels in cell membranes may be responsible for the multi-organ pathology observed in systemic lupus erythematosus patients, particularly neurological, cardiac and nephritic. Data from a different study conducted by the author suggests that latent and persistent viruses are reactivated in active lupus. This activation could be the result of the toxin's ability to act as an immune modulator, or its ability to act as a transactivating factor.
Url:
DOI: 10.1016/S0306-9877(96)90084-5
Affiliations:
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Mitchell</name><affiliation wicri:level="4"><orgName type="university">Université de Californie du Sud</orgName><country>États-Unis</country><placeName><settlement type="city">Los Angeles</settlement><region type="state">Californie</region></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j">Medical Hypotheses</title><title level="j" type="abbrev">YMEHY</title><idno type="ISSN">0306-9877</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1996">1996</date><biblScope unit="volume">47</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="217">217</biblScope><biblScope unit="page" to="225">225</biblScope></imprint><idno type="ISSN">0306-9877</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0306-9877</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Acad</term><term>Acetylcholine release</term><term>Antibody formation</term><term>Arthr rheum</term><term>Biochem biophys</term><term>Biol</term><term>Biol chem</term><term>Catecholamine secretion</term><term>Cell activation</term><term>Cell biol</term><term>Cell function</term><term>Cell membranes</term><term>Channel blocker</term><term>Clin</term><term>Clin immunol</term><term>Disease activity</term><term>Erythematosus</term><term>Frog lens</term><term>Herpes</term><term>Herpes simplex virus</term><term>Herpesviruses</term><term>Immune</term><term>Immune dysregulation</term><term>Immunol</term><term>Immunoregulatory subsets</term><term>Inhibitory activity</term><term>Interleukin</term><term>Kinase</term><term>Kinase activity</term><term>Long terminal</term><term>Lupus</term><term>Lupus erythematosus</term><term>Lymphocyte</term><term>Marine toxin</term><term>Marine toxins</term><term>Medical hypotheses</term><term>Memory phenotype</term><term>Okadaic</term><term>Okadaic acid</term><term>Okadaic toxin</term><term>Other diseases</term><term>Pathway</term><term>Patients exhibit</term><term>Persistent viruses</term><term>Phenotype</term><term>Phosphatase</term><term>Phosphatase inhibition</term><term>Phosphatase inhibitor</term><term>Phosphorylation</term><term>Preliminary experiment</term><term>Proc nail acad</term><term>Proc natl acad</term><term>Promoter</term><term>Protein phosphatases</term><term>Protein phosphorylation</term><term>Protein tyrosine kinase</term><term>Recent advances</term><term>Receptor</term><term>Repressive activity</term><term>Retinoblastoma gene product</term><term>Rheum</term><term>Rheumatoid arthritis</term><term>Serine</term><term>Signal transduction</term><term>Simplex</term><term>Sodium channels</term><term>Soluble receptor</term><term>Soluble receptors</term><term>Specific abnormalities</term><term>Systemic</term><term>Systemic lupus erythematosus</term><term>Systemic lupus erythematosus patients</term><term>Target cells</term><term>Toxin</term><term>Tumor necrosis factor</term><term>Tyrosine</term><term>Tyrosine phosphatase</term><term>Viral</term><term>Viral protein</term><term>Viral proteins</term><term>Virol</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Preliminary evidence suggests there is a toxin in the sera of systemic lupus erythematosus patients which reacts with a commercial enzyme-linked immunosorbent assay kit for the detection of the marine toxin, okadaic acid. Data is presented which supports the hypothesis that an okadaic acid-like toxin may be the principle agent of lymphocyte dysregulation in systemic lupus erythematosus and other immune-dysreguaated states. The okadaic acid-like toxin can produce the specific abnormalities in T-lymphocyte phenotype and function typical of systemic lupus erythematosus, principally through its ability to inhibit serine/threonine phosphatases necessary for secondary signalling processes, and through its ability to inhibit calcium which is crucial to protein kinase C-mediated signalling of T-lymphocytes. The disruption probably occurs through the protein tyrosine kinase p56lck pathway crucial for IL-2. Additionally, the toxin's ability to disrupt voltage-sensitive ion channels in cell membranes may be responsible for the multi-organ pathology observed in systemic lupus erythematosus patients, particularly neurological, cardiac and nephritic. Data from a different study conducted by the author suggests that latent and persistent viruses are reactivated in active lupus. This activation could be the result of the toxin's ability to act as an immune modulator, or its ability to act as a transactivating factor.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Californie</li></region><settlement><li>Los Angeles</li></settlement><orgName><li>Université de Californie du Sud</li></orgName></list><tree><country name="États-Unis"><region name="Californie"><name sortKey="Mitchell, T M" sort="Mitchell, T M" uniqKey="Mitchell T" first="T. M." last="Mitchell">T. M. Mitchell</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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