'Classic' Anti-Neutrophil Cytoplasmic Autoantibodies (cANCA), 'Wegener's Autoantigen' and Their Immunopathogenic Role in Wegener's Granulomatosis
Identifieur interne : 001689 ( Istex/Corpus ); précédent : 001688; suivant : 001690'Classic' Anti-Neutrophil Cytoplasmic Autoantibodies (cANCA), 'Wegener's Autoantigen' and Their Immunopathogenic Role in Wegener's Granulomatosis
Auteurs : Wolfgang L. Gross ; Elena Csernok ; Brigitte K. FleschSource :
- Journal of Autoimmunity [ 0896-8411 ] ; 1993.
Abstract
Abstract: Wegener's autoantigen (WA), a 29 kD multifunctional protein, is the principal target antigen of autoantibodies associated with Wegener's granulomatosis (WG). WA was first identified as proteinase 3 (PR3), which is now known to be identical with myeloblastin and AGP7. Like other lysosomal proteins, WA/PR3 displays enzymatic activity, differentiation factor activity for myeloid precursor cells, and antimicrobial functions. Neutrophilic polymorphonuclear leukocytes (PMN) and a subpopulation of monocytes contain high levels of WA/PR3 in their myeloperoxidase-positive granules. The autoantibodies from WG sera produce a finely granular, centrally accentuated fluorescence pattern on PMN and monocytes and have been designated 'classic' pattern antineutrophil cytoplasmic autoantibodies (cANCA). However, PMN/monocyte activation (in vitro/ex vivo) is associated with the translocation of WA/PR3 on the cytoplasm membrane. WA/PR3 is accessible to the WG-associated autoantibody: cANCA stimulate cytokine-preactivated PMN to produce oxygen radicals and to degranulate. Furthermore, cANCA interfere with the biological functions of WA/PR3 (e.g. inhibition of elastinolytic activity). Hence, cANCA represents not only the best seromarker for WG so far available, but several lines of evidence indicate that the autoantibodies against WA/PR3 play a major role in the pathogenesis of this enigmatic disease.
Url:
DOI: 10.1006/jaut.1993.1015
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Gross</name><affiliation><mods:affiliation>Medical University in Lübeck, Department of Clinical Rheumatology, and Rhemaklinik Bad Bramstedt, Germany</mods:affiliation></affiliation></author><author><name sortKey="Csernok, Elena" sort="Csernok, Elena" uniqKey="Csernok E" first="Elena" last="Csernok">Elena Csernok</name><affiliation><mods:affiliation>Medical University in Lübeck, Department of Clinical Rheumatology, and Rhemaklinik Bad Bramstedt, Germany</mods:affiliation></affiliation></author><author><name sortKey="Flesch, Brigitte K" sort="Flesch, Brigitte K" uniqKey="Flesch B" first="Brigitte K." last="Flesch">Brigitte K. Flesch</name><affiliation><mods:affiliation>Medical University in Lübeck, Department of Clinical Rheumatology, and Rhemaklinik Bad Bramstedt, Germany</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:DD014ECDA9AFA044D59DB02C001A5B7154E116EC</idno><date when="1993" year="1993">1993</date><idno type="doi">10.1006/jaut.1993.1015</idno><idno type="url">https://api.istex.fr/ark:/67375/6H6-X1WXBNS4-N/fulltext.pdf</idno><idno type="wicri:Area/Istex/Corpus">001689</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">001689</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">'Classic' Anti-Neutrophil Cytoplasmic Autoantibodies (cANCA), 'Wegener's Autoantigen' and Their Immunopathogenic Role in Wegener's Granulomatosis</title><author><name sortKey="Gross, Wolfgang L" sort="Gross, Wolfgang L" uniqKey="Gross W" first="Wolfgang L." last="Gross">Wolfgang L. Gross</name><affiliation><mods:affiliation>Medical University in Lübeck, Department of Clinical Rheumatology, and Rhemaklinik Bad Bramstedt, Germany</mods:affiliation></affiliation></author><author><name sortKey="Csernok, Elena" sort="Csernok, Elena" uniqKey="Csernok E" first="Elena" last="Csernok">Elena Csernok</name><affiliation><mods:affiliation>Medical University in Lübeck, Department of Clinical Rheumatology, and Rhemaklinik Bad Bramstedt, Germany</mods:affiliation></affiliation></author><author><name sortKey="Flesch, Brigitte K" sort="Flesch, Brigitte K" uniqKey="Flesch B" first="Brigitte K." last="Flesch">Brigitte K. Flesch</name><affiliation><mods:affiliation>Medical University in Lübeck, Department of Clinical Rheumatology, and Rhemaklinik Bad Bramstedt, Germany</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of Autoimmunity</title><title level="j" type="abbrev">YJAUT</title><idno type="ISSN">0896-8411</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1993">1993</date><biblScope unit="volume">6</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="171">171</biblScope><biblScope unit="page" to="184">184</biblScope></imprint><idno type="ISSN">0896-8411</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0896-8411</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Wegener's autoantigen (WA), a 29 kD multifunctional protein, is the principal target antigen of autoantibodies associated with Wegener's granulomatosis (WG). WA was first identified as proteinase 3 (PR3), which is now known to be identical with myeloblastin and AGP7. Like other lysosomal proteins, WA/PR3 displays enzymatic activity, differentiation factor activity for myeloid precursor cells, and antimicrobial functions. Neutrophilic polymorphonuclear leukocytes (PMN) and a subpopulation of monocytes contain high levels of WA/PR3 in their myeloperoxidase-positive granules. The autoantibodies from WG sera produce a finely granular, centrally accentuated fluorescence pattern on PMN and monocytes and have been designated 'classic' pattern antineutrophil cytoplasmic autoantibodies (cANCA). However, PMN/monocyte activation (in vitro/ex vivo) is associated with the translocation of WA/PR3 on the cytoplasm membrane. WA/PR3 is accessible to the WG-associated autoantibody: cANCA stimulate cytokine-preactivated PMN to produce oxygen radicals and to degranulate. Furthermore, cANCA interfere with the biological functions of WA/PR3 (e.g. inhibition of elastinolytic activity). Hence, cANCA represents not only the best seromarker for WG so far available, but several lines of evidence indicate that the autoantibodies against WA/PR3 play a major role in the pathogenesis of this enigmatic disease.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>Wolfgang L. Gross</name><affiliations><json:string>Medical University in Lübeck, Department of Clinical Rheumatology, and Rhemaklinik Bad Bramstedt, Germany</json:string></affiliations></json:item><json:item><name>Elena Csernok</name><affiliations><json:string>Medical University in Lübeck, Department of Clinical Rheumatology, and Rhemaklinik Bad Bramstedt, Germany</json:string></affiliations></json:item><json:item><name>Brigitte K. 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The autoantibodies from WG sera produce a finely granular, centrally accentuated fluorescence pattern on PMN and monocytes and have been designated 'classic' pattern antineutrophil cytoplasmic autoantibodies (cANCA). However, PMN/monocyte activation (in vitro/ex vivo) is associated with the translocation of WA/PR3 on the cytoplasm membrane. WA/PR3 is accessible to the WG-associated autoantibody: cANCA stimulate cytokine-preactivated PMN to produce oxygen radicals and to degranulate. Furthermore, cANCA interfere with the biological functions of WA/PR3 (e.g. inhibition of elastinolytic activity). 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WA was first identified as proteinase 3 (PR3), which is now known to be identical with myeloblastin and AGP7. Like other lysosomal proteins, WA/PR3 displays enzymatic activity, differentiation factor activity for myeloid precursor cells, and antimicrobial functions. Neutrophilic polymorphonuclear leukocytes (PMN) and a subpopulation of monocytes contain high levels of WA/PR3 in their myeloperoxidase-positive granules. The autoantibodies from WG sera produce a finely granular, centrally accentuated fluorescence pattern on PMN and monocytes and have been designated 'classic' pattern antineutrophil cytoplasmic autoantibodies (cANCA). However, PMN/monocyte activation (in vitro/ex vivo) is associated with the translocation of WA/PR3 on the cytoplasm membrane. WA/PR3 is accessible to the WG-associated autoantibody: cANCA stimulate cytokine-preactivated PMN to produce oxygen radicals and to degranulate. Furthermore, cANCA interfere with the biological functions of WA/PR3 (e.g. inhibition of elastinolytic activity). Hence, cANCA represents not only the best seromarker for WG so far available, but several lines of evidence indicate that the autoantibodies against WA/PR3 play a major role in the pathogenesis of this enigmatic disease.</p></abstract></profileDesc><revisionDesc><change when="1993">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-X1WXBNS4-N/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier converted-article found"><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" xml:lang="en"><item-info><jid>YJAUT</jid><aid>71015</aid><ce:pii>S0896-8411(83)71015-2</ce:pii><ce:doi>10.1006/jaut.1993.1015</ce:doi><ce:copyright type="full-transfer" year="1993">Academic Press</ce:copyright></item-info><head><ce:dochead><ce:textfn>Regular Article</ce:textfn></ce:dochead><ce:title>'Classic' Anti-Neutrophil Cytoplasmic Autoantibodies (cANCA), 'Wegener's Autoantigen' and Their Immunopathogenic Role in Wegener's Granulomatosis</ce:title><ce:author-group><ce:author><ce:given-name>Wolfgang L.</ce:given-name><ce:surname>Gross</ce:surname></ce:author><ce:author><ce:given-name>Elena</ce:given-name><ce:surname>Csernok</ce:surname></ce:author><ce:author><ce:given-name>Brigitte K.</ce:given-name><ce:surname>Flesch</ce:surname></ce:author><ce:affiliation><ce:textfn>Medical University in Lübeck, Department of Clinical Rheumatology, and Rhemaklinik Bad Bramstedt, Germany</ce:textfn></ce:affiliation></ce:author-group><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>Wegener's autoantigen (WA), a 29 kD multifunctional protein, is the principal target antigen of autoantibodies associated with Wegener's granulomatosis (WG). WA was first identified as proteinase 3 (PR3), which is now known to be identical with myeloblastin and AGP7. Like other lysosomal proteins, WA/PR3 displays enzymatic activity, differentiation factor activity for myeloid precursor cells, and antimicrobial functions. Neutrophilic polymorphonuclear leukocytes (PMN) and a subpopulation of monocytes contain high levels of WA/PR3 in their myeloperoxidase-positive granules. The autoantibodies from WG sera produce a finely granular, centrally accentuated fluorescence pattern on PMN and monocytes and have been designated 'classic' pattern antineutrophil cytoplasmic autoantibodies (cANCA). However, PMN/monocyte activation (<ce:italic>in vitro/ex vivo</ce:italic>) is associated with the translocation of WA/PR3 on the cytoplasm membrane. WA/PR3 is accessible to the WG-associated autoantibody: cANCA stimulate cytokine-preactivated PMN to produce oxygen radicals and to degranulate. Furthermore, cANCA interfere with the biological functions of WA/PR3 (e.g. inhibition of elastinolytic activity). Hence, cANCA represents not only the best seromarker for WG so far available, but several lines of evidence indicate that the autoantibodies against WA/PR3 play a major role in the pathogenesis of this enigmatic disease.</ce:simple-para></ce:abstract-sec></ce:abstract></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>'Classic' Anti-Neutrophil Cytoplasmic Autoantibodies (cANCA), 'Wegener's Autoantigen' and Their Immunopathogenic Role in Wegener's Granulomatosis</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>'Classic' Anti-Neutrophil Cytoplasmic Autoantibodies (cANCA), 'Wegener's Autoantigen' and Their Immunopathogenic Role in Wegener's Granulomatosis</title></titleInfo><name type="personal"><namePart type="given">Wolfgang L.</namePart><namePart type="family">Gross</namePart><affiliation>Medical University in Lübeck, Department of Clinical Rheumatology, and Rhemaklinik Bad Bramstedt, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Elena</namePart><namePart type="family">Csernok</namePart><affiliation>Medical University in Lübeck, Department of Clinical Rheumatology, and Rhemaklinik Bad Bramstedt, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Brigitte K.</namePart><namePart type="family">Flesch</namePart><affiliation>Medical University in Lübeck, Department of Clinical Rheumatology, and Rhemaklinik Bad Bramstedt, Germany</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">1993</dateIssued><copyrightDate encoding="w3cdtf">1993</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><abstract lang="en">Abstract: Wegener's autoantigen (WA), a 29 kD multifunctional protein, is the principal target antigen of autoantibodies associated with Wegener's granulomatosis (WG). WA was first identified as proteinase 3 (PR3), which is now known to be identical with myeloblastin and AGP7. Like other lysosomal proteins, WA/PR3 displays enzymatic activity, differentiation factor activity for myeloid precursor cells, and antimicrobial functions. Neutrophilic polymorphonuclear leukocytes (PMN) and a subpopulation of monocytes contain high levels of WA/PR3 in their myeloperoxidase-positive granules. The autoantibodies from WG sera produce a finely granular, centrally accentuated fluorescence pattern on PMN and monocytes and have been designated 'classic' pattern antineutrophil cytoplasmic autoantibodies (cANCA). However, PMN/monocyte activation (in vitro/ex vivo) is associated with the translocation of WA/PR3 on the cytoplasm membrane. WA/PR3 is accessible to the WG-associated autoantibody: cANCA stimulate cytokine-preactivated PMN to produce oxygen radicals and to degranulate. Furthermore, cANCA interfere with the biological functions of WA/PR3 (e.g. inhibition of elastinolytic activity). Hence, cANCA represents not only the best seromarker for WG so far available, but several lines of evidence indicate that the autoantibodies against WA/PR3 play a major role in the pathogenesis of this enigmatic disease.</abstract><note type="content">Section title: Regular Article</note><relatedItem type="host"><titleInfo><title>Journal of Autoimmunity</title></titleInfo><titleInfo type="abbreviated"><title>YJAUT</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">1993</dateIssued></originInfo><identifier type="ISSN">0896-8411</identifier><identifier type="PII">S0896-8411(00)X0051-0</identifier><part><date>1993</date><detail type="volume"><number>6</number><caption>vol.</caption></detail><detail type="issue"><number>2</number><caption>no.</caption></detail><extent unit="issue-pages"><start>131</start><end>264</end></extent><extent unit="pages"><start>171</start><end>184</end></extent></part></relatedItem><identifier type="istex">DD014ECDA9AFA044D59DB02C001A5B7154E116EC</identifier><identifier type="ark">ark:/67375/6H6-X1WXBNS4-N</identifier><identifier type="DOI">10.1006/jaut.1993.1015</identifier><identifier type="PII">S0896-8411(83)71015-2</identifier><accessCondition type="use and reproduction" contentType="copyright">©1993 Academic Press</accessCondition><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><recordOrigin>Academic Press, ©1993</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-X1WXBNS4-N/record.json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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