Okadaic acid-like toxin in systemic lupus erythematosus patients: Hypothesis for toxin-induced pathology, immune dysregulation, and transactivation of herpesviruses
Identifieur interne : 000D10 ( Istex/Corpus ); précédent : 000D09; suivant : 000D11Okadaic acid-like toxin in systemic lupus erythematosus patients: Hypothesis for toxin-induced pathology, immune dysregulation, and transactivation of herpesviruses
Auteurs : T. M. MitchellSource :
- 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
Links to Exploration step
ISTEX:58CFD4324209046BE45271C7D8B50D6D79BA2594Le document en format XML
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Mitchell</name><affiliation><mods:affiliation>University of Southern California, 830 Childs Way, Box 415, Los Angeles, CA 90089, USA (Fax: (+1) (213) 665-7729)</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:58CFD4324209046BE45271C7D8B50D6D79BA2594</idno><date when="1996" year="1996">1996</date><idno type="doi">10.1016/S0306-9877(96)90084-5</idno><idno type="url">https://api.istex.fr/ark:/67375/6H6-3B43QJKM-K/fulltext.pdf</idno><idno type="wicri:Area/Istex/Corpus">000D10</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">000D10</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a">Okadaic acid-like toxin in systemic lupus erythematosus patients: Hypothesis for toxin-induced pathology, immune dysregulation, and transactivation of herpesviruses</title><author><name sortKey="Mitchell, T M" sort="Mitchell, T M" uniqKey="Mitchell T" first="T. M." last="Mitchell">T. M. Mitchell</name><affiliation><mods:affiliation>University of Southern California, 830 Childs Way, Box 415, Los Angeles, CA 90089, USA (Fax: (+1) (213) 665-7729)</mods:affiliation></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><istex><corpusName>elsevier</corpusName><keywords><teeft><json:string>lupus</json:string><json:string>erythematosus</json:string><json:string>receptor</json:string><json:string>okadaic</json:string><json:string>systemic lupus erythematosus</json:string><json:string>phosphorylation</json:string><json:string>phosphatase</json:string><json:string>toxin</json:string><json:string>lymphocyte</json:string><json:string>immunol</json:string><json:string>herpesviruses</json:string><json:string>kinase</json:string><json:string>clin</json:string><json:string>herpes</json:string><json:string>interleukin</json:string><json:string>phenotype</json:string><json:string>okadaic toxin</json:string><json:string>immune</json:string><json:string>okadaic acid</json:string><json:string>serine</json:string><json:string>biol</json:string><json:string>virol</json:string><json:string>viral</json:string><json:string>acad</json:string><json:string>pathway</json:string><json:string>lupus erythematosus</json:string><json:string>systemic lupus erythematosus patients</json:string><json:string>systemic</json:string><json:string>biol chem</json:string><json:string>arthr rheum</json:string><json:string>immune dysregulation</json:string><json:string>herpes simplex virus</json:string><json:string>tumor necrosis factor</json:string><json:string>tyrosine phosphatase</json:string><json:string>proc natl acad</json:string><json:string>simplex</json:string><json:string>rheum</json:string><json:string>promoter</json:string><json:string>channel blocker</json:string><json:string>patients exhibit</json:string><json:string>cell function</json:string><json:string>viral proteins</json:string><json:string>protein tyrosine kinase</json:string><json:string>disease activity</json:string><json:string>antibody formation</json:string><json:string>cell membranes</json:string><json:string>protein phosphorylation</json:string><json:string>marine toxins</json:string><json:string>signal transduction</json:string><json:string>persistent viruses</json:string><json:string>tyrosine</json:string><json:string>soluble receptors</json:string><json:string>phosphatase inhibition</json:string><json:string>medical hypotheses</json:string><json:string>specific abnormalities</json:string><json:string>cell activation</json:string><json:string>viral protein</json:string><json:string>inhibitory activity</json:string><json:string>repressive activity</json:string><json:string>preliminary experiment</json:string><json:string>other diseases</json:string><json:string>immunoregulatory subsets</json:string><json:string>sodium channels</json:string><json:string>acetylcholine release</json:string><json:string>phosphatase inhibitor</json:string><json:string>marine toxin</json:string><json:string>clin immunol</json:string><json:string>rheumatoid arthritis</json:string><json:string>catecholamine secretion</json:string><json:string>target cells</json:string><json:string>cell biol</json:string><json:string>frog lens</json:string><json:string>memory phenotype</json:string><json:string>protein phosphatases</json:string><json:string>soluble receptor</json:string><json:string>proc nail acad</json:string><json:string>kinase activity</json:string><json:string>biochem biophys</json:string><json:string>recent advances</json:string><json:string>retinoblastoma gene product</json:string><json:string>long terminal</json:string></teeft></keywords><author><json:item><name>T.M. Mitchell</name><affiliations><json:string>University of Southern California, 830 Childs Way, Box 415, Los Angeles, CA 90089, USA (Fax: (+1) (213) 665-7729)</json:string></affiliations></json:item></author><arkIstex>ark:/67375/6H6-3B43QJKM-K</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>Full-length article</json:string></originalGenre><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.</abstract><qualityIndicators><score>9.4</score><pdfWordCount>5974</pdfWordCount><pdfCharCount>37730</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>9</pdfPageCount><pdfPageSize>540 x 720 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractWordCount>200</abstractWordCount><abstractCharCount>1434</abstractCharCount><keywordCount>0</keywordCount></qualityIndicators><title>Okadaic acid-like toxin in systemic lupus erythematosus patients: Hypothesis for toxin-induced pathology, immune dysregulation, and transactivation of herpesviruses</title><pmid><json:string>8898323</json:string></pmid><pii><json:string>S0306-9877(96)90084-5</json:string></pii><genre><json:string>research-article</json:string></genre><serie><title>(8)</title><language><json:string>unknown</json:string></language><volume>78</volume><pages><first>4950</first><last>4954</last></pages></serie><host><title>Medical Hypotheses</title><language><json:string>unknown</json:string></language><publicationDate>1996</publicationDate><issn><json:string>0306-9877</json:string></issn><pii><json:string>S0306-9877(00)X0296-4</json:string></pii><volume>47</volume><issue>3</issue><pages><first>217</first><last>225</last></pages><genre><json:string>journal</json:string></genre></host><namedEntities><unitex><date><json:string>1996</json:string></date><geogName></geogName><orgName><json:string>University of Southern California</json:string><json:string>American College of Rheumatology</json:string><json:string>Specialty Laboratories, Santa Monica</json:string></orgName><orgName_funder></orgName_funder><orgName_provider></orgName_provider><persName><json:string>Nagelkerken</json:string><json:string>Henkel</json:string><json:string>Huijbregts</json:string><json:string>Interleukin</json:string><json:string>Minh-Duc Nguyen</json:string><json:string>Sushil Mohapatra</json:string><json:string>Bajpai</json:string><json:string>John Vaughn</json:string><json:string>Daniel J. 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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.</p></abstract></profileDesc><revisionDesc><change when="1996">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-3B43QJKM-K/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: tail"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla"><item-info><jid>YMEHY</jid><aid>96900845</aid><ce:pii>S0306-9877(96)90084-5</ce:pii><ce:doi>10.1016/S0306-9877(96)90084-5</ce:doi><ce:copyright type="unknown" year="1996"></ce:copyright></item-info><head><ce:title>Okadaic acid-like toxin in systemic lupus erythematosus patients: Hypothesis for toxin-induced pathology, immune dysregulation, and transactivation of herpesviruses</ce:title><ce:author-group><ce:author><ce:given-name>T.M.</ce:given-name><ce:surname>Mitchell</ce:surname></ce:author><ce:affiliation><ce:textfn>University of Southern California, 830 Childs Way, Box 415, Los Angeles, CA 90089, USA (Fax: (+1) (213) 665-7729)</ce:textfn></ce:affiliation></ce:author-group><ce:date-received day="1" month="6" year="1995"></ce:date-received><ce:date-accepted day="2" month="10" year="1995"></ce:date-accepted><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>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.</ce:simple-para><ce:simple-para>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 p56<ce:sup>lck</ce:sup> 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.</ce:simple-para><ce:simple-para>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.</ce:simple-para></ce:abstract-sec></ce:abstract></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Okadaic acid-like toxin in systemic lupus erythematosus patients: Hypothesis for toxin-induced pathology, immune dysregulation, and transactivation of herpesviruses</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Okadaic acid-like toxin in systemic lupus erythematosus patients: Hypothesis for toxin-induced pathology, immune dysregulation, and transactivation of herpesviruses</title></titleInfo><name type="personal"><namePart type="given">T.M.</namePart><namePart type="family">Mitchell</namePart><affiliation>University of Southern California, 830 Childs Way, Box 415, Los Angeles, CA 90089, USA (Fax: (+1) (213) 665-7729)</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1996</dateIssued><copyrightDate encoding="w3cdtf">1996</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><abstract 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.</abstract><relatedItem type="host"><titleInfo><title>Medical Hypotheses</title></titleInfo><titleInfo type="abbreviated"><title>YMEHY</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1996</dateIssued></originInfo><identifier type="ISSN">0306-9877</identifier><identifier type="PII">S0306-9877(00)X0296-4</identifier><part><date>1996</date><detail type="volume"><number>47</number><caption>vol.</caption></detail><detail type="issue"><number>3</number><caption>no.</caption></detail><extent unit="issue-pages"><start>179</start><end>255</end></extent><extent unit="pages"><start>217</start><end>225</end></extent></part></relatedItem><identifier type="istex">58CFD4324209046BE45271C7D8B50D6D79BA2594</identifier><identifier type="ark">ark:/67375/6H6-3B43QJKM-K</identifier><identifier type="DOI">10.1016/S0306-9877(96)90084-5</identifier><identifier type="PII">S0306-9877(96)90084-5</identifier><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M">elsevier</recordContentSource></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-3B43QJKM-K/record.json</uri></json:item></metadata></istex></record>Pour manipuler ce document sous Unix (Dilib)
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