Influenza A virus hemagglutinin is a B cell-superstimulatory lectin
Identifieur interne : 001218 ( Istex/Corpus ); précédent : 001217; suivant : 001219Influenza A virus hemagglutinin is a B cell-superstimulatory lectin
Auteurs : Ortwin Rott ; Jeannine Charreire ; Evelyne CashSource :
- Medical Microbiology and Immunology [ 0300-8584 ] ; 1996-02-01.
English descriptors
- KwdEn :
- Teeft :
- Aggregation, Amino acids, Anders, Antigenic site, Binding site, Cell activation, Cell aggregates, Cell aggregation, Cell mitogenicity, Cell proliferation, Cell stimulation, Cell surface marker expression, Chimeric, Control cultures, Culture medium, Culture period, Culture plates, Different viruses, Direct interaction, Fusion peptide, Generous gift, Globular region, Glycoprotein, Hemagglutinin, High degree, Homotypic aggregation, Hypervariable loop region, Immunol, Influenza, Influenza virus, Influenza virus hemagglutinin, Influenza virus transfectants, Influenza viruses, Inhibitor, Inhibitors tunicamycin, Light microscopy, Loop region, Lymphocyte, Lymphocyte activation, Lymphocyte receptors, Microtiter plates, Mitogenic activity, Molecular basis, Mutant viruses, Neuraminidase treatment, Other experiments, Palese, Proliferative, Proliferative responses, Reassortant viruses, Receptor, Receptor binding, Receptor determinants, Responder, Responder cells, Rott, Simultaneous addition, Sinai school, Subtypes, Terminal sialic acid residues, Triplicate determinations, Vast differences, Viral, Viral envelope protein, Virus, Virus infection, Wild type.
Abstract
Abstract: Influenza A viruses display T cell-independent polyclonal B cell-activating properties which are mediated by the B cell-superstimulatory envelope glycoprotein hemagglutinin (HA). In this report, the receptor-binding requirements for B cell activation by influenza viruses were expected. Neuraminidase treatment of resting mature B cells from BALB/c mice abrogated late (proliferation/immunoglobulin synthesis), early (up-regulation of cell surface markers, including CD25, B220, and B7-1) and veryearly events (homotypic adhesion) in virus-responding B lymphocytes. Similarly, pretreatment of murine responder cells with different inhibitors ofN-glycosylation (tunicamycin, deoxymannojirimycin) significantly suppressed subsequent B lymphocyte activation by HA, but not control responses to lipopolysaccharide or anti-μ. Assays with chimeric HA transfectants, expressing the loop region of epitope B (amino acids 155–160) of the globular head of H2 (high B cell-stimulatory subtype) or H3 (medium-stimulatory subtype) on the protein backbone of a low-stimulatory subtype (H1) failed to alter the B cell-stimulatory activity of the virus, suggesting that the hypervariable loop region is not crucial in determining the B cell-activating properties of the protein. Collectively, our results imply that the B cell-superstimulatory function of influenza virus HA is not mediated by a direct protein/protein interaction, but via binding of HA to terminal sialic acid residues on cell surface receptor glycoproteins. These findings identify the influenza virus HA glycoprotein as the first viral lectin with lymphocyte-activating properties.
Url:
DOI: 10.1007/BF02456134
Links to Exploration step
ISTEX:D7310E89F1F62F7DF84F75B4B166EAA695634DE0Le document en format XML
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In this report, the receptor-binding requirements for B cell activation by influenza viruses were expected. Neuraminidase treatment of resting mature B cells from BALB/c mice abrogated late (proliferation/immunoglobulin synthesis), early (up-regulation of cell surface markers, including CD25, B220, and B7-1) and veryearly events (homotypic adhesion) in virus-responding B lymphocytes. Similarly, pretreatment of murine responder cells with different inhibitors ofN-glycosylation (tunicamycin, deoxymannojirimycin) significantly suppressed subsequent B lymphocyte activation by HA, but not control responses to lipopolysaccharide or anti-μ. Assays with chimeric HA transfectants, expressing the loop region of epitope B (amino acids 155–160) of the globular head of H2 (high B cell-stimulatory subtype) or H3 (medium-stimulatory subtype) on the protein backbone of a low-stimulatory subtype (H1) failed to alter the B cell-stimulatory activity of the virus, suggesting that the hypervariable loop region is not crucial in determining the B cell-activating properties of the protein. Collectively, our results imply that the B cell-superstimulatory function of influenza virus HA is not mediated by a direct protein/protein interaction, but via binding of HA to terminal sialic acid residues on cell surface receptor glycoproteins. These findings identify the influenza virus HA glycoprotein as the first viral lectin with lymphocyte-activating properties.</div></front></TEI><istex><corpusName>springer-journals</corpusName><keywords><teeft><json:string>lymphocyte</json:string><json:string>receptor</json:string><json:string>rott</json:string><json:string>glycoprotein</json:string><json:string>influenza virus</json:string><json:string>hemagglutinin</json:string><json:string>influenza</json:string><json:string>influenza viruses</json:string><json:string>chimeric</json:string><json:string>cell activation</json:string><json:string>immunol</json:string><json:string>proliferative</json:string><json:string>loop region</json:string><json:string>responder</json:string><json:string>viral</json:string><json:string>subtypes</json:string><json:string>palese</json:string><json:string>aggregation</json:string><json:string>proliferative responses</json:string><json:string>responder cells</json:string><json:string>triplicate determinations</json:string><json:string>virus</json:string><json:string>viral envelope protein</json:string><json:string>neuraminidase treatment</json:string><json:string>cell proliferation</json:string><json:string>cell mitogenicity</json:string><json:string>lymphocyte activation</json:string><json:string>reassortant viruses</json:string><json:string>different viruses</json:string><json:string>homotypic aggregation</json:string><json:string>wild type</json:string><json:string>binding site</json:string><json:string>cell aggregates</json:string><json:string>influenza virus hemagglutinin</json:string><json:string>culture medium</json:string><json:string>amino acids</json:string><json:string>generous gift</json:string><json:string>globular region</json:string><json:string>sinai school</json:string><json:string>inhibitors tunicamycin</json:string><json:string>hypervariable loop region</json:string><json:string>culture plates</json:string><json:string>culture period</json:string><json:string>molecular basis</json:string><json:string>receptor determinants</json:string><json:string>simultaneous addition</json:string><json:string>direct interaction</json:string><json:string>antigenic site</json:string><json:string>control cultures</json:string><json:string>virus infection</json:string><json:string>cell surface marker expression</json:string><json:string>terminal sialic acid residues</json:string><json:string>lymphocyte receptors</json:string><json:string>microtiter plates</json:string><json:string>cell stimulation</json:string><json:string>influenza virus transfectants</json:string><json:string>mutant viruses</json:string><json:string>cell aggregation</json:string><json:string>mitogenic activity</json:string><json:string>vast differences</json:string><json:string>light microscopy</json:string><json:string>receptor binding</json:string><json:string>high degree</json:string><json:string>fusion peptide</json:string><json:string>other experiments</json:string><json:string>anders</json:string><json:string>inhibitor</json:string></teeft></keywords><author><json:item><name>Ortwin Rott</name><affiliations><json:string>INSERM U. 283, Hôpital Cochin, Université René Descartes, 27 rue du Fg. St.-Jacques, F-75674, Paris, France</json:string></affiliations></json:item><json:item><name>Jeannine Charreire</name><affiliations><json:string>INSERM U. 283, Hôpital Cochin, Université René Descartes, 27 rue du Fg. St.-Jacques, F-75674, Paris, France</json:string></affiliations></json:item><json:item><name>Evelyne Cash</name><affiliations><json:string>INSERM U. 283, Hôpital Cochin, Université René Descartes, 27 rue du Fg. 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Neuraminidase treatment of resting mature B cells from BALB/c mice abrogated late (proliferation/immunoglobulin synthesis), early (up-regulation of cell surface markers, including CD25, B220, and B7-1) and veryearly events (homotypic adhesion) in virus-responding B lymphocytes. Similarly, pretreatment of murine responder cells with different inhibitors ofN-glycosylation (tunicamycin, deoxymannojirimycin) significantly suppressed subsequent B lymphocyte activation by HA, but not control responses to lipopolysaccharide or anti-μ. Assays with chimeric HA transfectants, expressing the loop region of epitope B (amino acids 155–160) of the globular head of H2 (high B cell-stimulatory subtype) or H3 (medium-stimulatory subtype) on the protein backbone of a low-stimulatory subtype (H1) failed to alter the B cell-stimulatory activity of the virus, suggesting that the hypervariable loop region is not crucial in determining the B cell-activating properties of the protein. Collectively, our results imply that the B cell-superstimulatory function of influenza virus HA is not mediated by a direct protein/protein interaction, but via binding of HA to terminal sialic acid residues on cell surface receptor glycoproteins. 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St.-Jacques, F-75674, Paris, France</affiliation></author><author xml:id="author-0001" corresp="yes"><persName><forename type="first">Jeannine</forename><surname>Charreire</surname></persName><affiliation>INSERM U. 283, Hôpital Cochin, Université René Descartes, 27 rue du Fg. St.-Jacques, F-75674, Paris, France</affiliation></author><author xml:id="author-0002"><persName><forename type="first">Evelyne</forename><surname>Cash</surname></persName><affiliation>INSERM U. 283, Hôpital Cochin, Université René Descartes, 27 rue du Fg. St.-Jacques, F-75674, Paris, France</affiliation></author><idno type="istex">D7310E89F1F62F7DF84F75B4B166EAA695634DE0</idno><idno type="ark">ark:/67375/1BB-RMF521W1-9</idno><idno type="DOI">10.1007/BF02456134</idno><idno type="article-id">BF02456134</idno><idno type="article-id">Art6</idno></analytic><monogr><title level="j">Medical Microbiology and Immunology</title><title level="j" type="abbrev">Med Microbiol Immunol</title><idno type="pISSN">0300-8584</idno><idno type="eISSN">1432-1831</idno><idno type="journal-ID">true</idno><idno type="issue-article-count">7</idno><idno type="volume-issue-count">4</idno><imprint><publisher>Springer-Verlag</publisher><pubPlace>Berlin/Heidelberg</pubPlace><date type="published" when="1996-02-01"></date><biblScope unit="volume">184</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="185">185</biblScope><biblScope unit="page" to="193">193</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1995-10-03</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Abstract: Influenza A viruses display T cell-independent polyclonal B cell-activating properties which are mediated by the B cell-superstimulatory envelope glycoprotein hemagglutinin (HA). In this report, the receptor-binding requirements for B cell activation by influenza viruses were expected. Neuraminidase treatment of resting mature B cells from BALB/c mice abrogated late (proliferation/immunoglobulin synthesis), early (up-regulation of cell surface markers, including CD25, B220, and B7-1) and veryearly events (homotypic adhesion) in virus-responding B lymphocytes. Similarly, pretreatment of murine responder cells with different inhibitors ofN-glycosylation (tunicamycin, deoxymannojirimycin) significantly suppressed subsequent B lymphocyte activation by HA, but not control responses to lipopolysaccharide or anti-μ. Assays with chimeric HA transfectants, expressing the loop region of epitope B (amino acids 155–160) of the globular head of H2 (high B cell-stimulatory subtype) or H3 (medium-stimulatory subtype) on the protein backbone of a low-stimulatory subtype (H1) failed to alter the B cell-stimulatory activity of the virus, suggesting that the hypervariable loop region is not crucial in determining the B cell-activating properties of the protein. Collectively, our results imply that the B cell-superstimulatory function of influenza virus HA is not mediated by a direct protein/protein interaction, but via binding of HA to terminal sialic acid residues on cell surface receptor glycoproteins. These findings identify the influenza virus HA glycoprotein as the first viral lectin with lymphocyte-activating properties.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Key words</head><item><term>Influenza virus</term></item><item><term>Superantigen</term></item><item><term>B cell activation</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Biomedicine</head><item><term>Immunology</term></item><item><term>Medical Microbiology</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1995-10-03">Created</change><change when="1996-02-01">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/1BB-RMF521W1-9/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus springer-journals not found" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="UTF-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//Springer-Verlag//DTD A++ V2.4//EN" URI="http://devel.springer.de/A++/V2.4/DTD/A++V2.4.dtd" name="istex:docType"></istex:docType><istex:document><Publisher><PublisherInfo><PublisherName>Springer-Verlag</PublisherName><PublisherLocation>Berlin/Heidelberg</PublisherLocation></PublisherInfo><Journal><JournalInfo JournalProductType="ArchiveJournal" NumberingStyle="Unnumbered"><JournalID>430</JournalID><JournalPrintISSN>0300-8584</JournalPrintISSN><JournalElectronicISSN>1432-1831</JournalElectronicISSN><JournalTitle>Medical Microbiology and Immunology</JournalTitle><JournalAbbreviatedTitle>Med Microbiol Immunol</JournalAbbreviatedTitle><JournalSubjectGroup><JournalSubject Type="Primary">Biomedicine</JournalSubject><JournalSubject Type="Secondary">Immunology</JournalSubject><JournalSubject Type="Secondary">Medical Microbiology</JournalSubject></JournalSubjectGroup></JournalInfo><Volume><VolumeInfo TocLevels="0" VolumeType="Regular"><VolumeIDStart>184</VolumeIDStart><VolumeIDEnd>184</VolumeIDEnd><VolumeIssueCount>4</VolumeIssueCount></VolumeInfo><Issue IssueType="Regular"><IssueInfo TocLevels="0"><IssueIDStart>4</IssueIDStart><IssueIDEnd>4</IssueIDEnd><IssueArticleCount>7</IssueArticleCount><IssueHistory><CoverDate><Year>1996</Year><Month>2</Month></CoverDate></IssueHistory><IssueCopyright><CopyrightHolderName>Springer-Verlag</CopyrightHolderName><CopyrightYear>1996</CopyrightYear></IssueCopyright></IssueInfo><Article ID="Art6"><ArticleInfo ArticleType="OriginalPaper" ContainsESM="No" Language="En" NumberingStyle="Unnumbered" TocLevels="0"><ArticleID>BF02456134</ArticleID><ArticleDOI>10.1007/BF02456134</ArticleDOI><ArticleSequenceNumber>6</ArticleSequenceNumber><ArticleTitle Language="En">Influenza A virus hemagglutinin is a B cell-superstimulatory lectin</ArticleTitle><ArticleCategory>Original Investigation</ArticleCategory><ArticleFirstPage>185</ArticleFirstPage><ArticleLastPage>193</ArticleLastPage><ArticleHistory><RegistrationDate><Year>2006</Year><Month>6</Month><Day>27</Day></RegistrationDate><Received><Year>1995</Year><Month>10</Month><Day>3</Day></Received></ArticleHistory><ArticleCopyright><CopyrightHolderName>Springer-Verlag</CopyrightHolderName><CopyrightYear>1996</CopyrightYear></ArticleCopyright><ArticleGrants Type="Regular"><MetadataGrant Grant="OpenAccess"></MetadataGrant><AbstractGrant Grant="OpenAccess"></AbstractGrant><BodyPDFGrant Grant="Restricted"></BodyPDFGrant><BodyHTMLGrant Grant="Restricted"></BodyHTMLGrant><BibliographyGrant Grant="Restricted"></BibliographyGrant><ESMGrant Grant="Restricted"></ESMGrant></ArticleGrants><ArticleContext><JournalID>430</JournalID><VolumeIDStart>184</VolumeIDStart><VolumeIDEnd>184</VolumeIDEnd><IssueIDStart>4</IssueIDStart><IssueIDEnd>4</IssueIDEnd></ArticleContext></ArticleInfo><ArticleHeader><AuthorGroup><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>Ortwin</GivenName><FamilyName>Rott</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1" CorrespondingAffiliationID="Aff1"><AuthorName DisplayOrder="Western"><GivenName>Jeannine</GivenName><FamilyName>Charreire</FamilyName></AuthorName><Contact><Phone>+33-1-42341829</Phone><Fax>+33-1-43261156</Fax></Contact></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>Evelyne</GivenName><FamilyName>Cash</FamilyName></AuthorName></Author><Affiliation ID="Aff1"><OrgDivision>INSERM U. 283, Hôpital Cochin</OrgDivision><OrgName>Université René Descartes</OrgName><OrgAddress><Street>27 rue du Fg. St.-Jacques</Street><Postcode>F-75674</Postcode><City>Paris</City><Country>France</Country></OrgAddress></Affiliation></AuthorGroup><Abstract ID="Abs1" Language="En"><Heading>Abstract</Heading><Para>Influenza A viruses display T cell-independent polyclonal B cell-activating properties which are mediated by the B cell-superstimulatory envelope glycoprotein hemagglutinin (HA). In this report, the receptor-binding requirements for B cell activation by influenza viruses were expected. Neuraminidase treatment of resting mature B cells from BALB/c mice abrogated late (proliferation/immunoglobulin synthesis), early (up-regulation of cell surface markers, including CD25, B220, and B7-1) and veryearly events (homotypic adhesion) in virus-responding B lymphocytes. Similarly, pretreatment of murine responder cells with different inhibitors of<Emphasis Type="Italic">N</Emphasis>-glycosylation (tunicamycin, deoxymannojirimycin) significantly suppressed subsequent B lymphocyte activation by HA, but not control responses to lipopolysaccharide or anti-μ. Assays with chimeric HA transfectants, expressing the loop region of epitope B (amino acids 155–160) of the globular head of H2 (high B cell-stimulatory subtype) or H3 (medium-stimulatory subtype) on the protein backbone of a low-stimulatory subtype (H1) failed to alter the B cell-stimulatory activity of the virus, suggesting that the hypervariable loop region is not crucial in determining the B cell-activating properties of the protein. Collectively, our results imply that the B cell-superstimulatory function of influenza virus HA is not mediated by a direct protein/protein interaction, but via binding of HA to terminal sialic acid residues on cell surface receptor glycoproteins. These findings identify the influenza virus HA glycoprotein as the first viral lectin with lymphocyte-activating properties.</Para></Abstract><KeywordGroup Language="En"><Heading>Key words</Heading><Keyword>Influenza virus</Keyword><Keyword>Superantigen</Keyword><Keyword>B cell activation</Keyword></KeywordGroup></ArticleHeader><NoBody></NoBody></Article></Issue></Volume></Journal></Publisher></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Influenza A virus hemagglutinin is a B cell-superstimulatory lectin</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Influenza A virus hemagglutinin is a B cell-superstimulatory lectin</title></titleInfo><name type="personal"><namePart type="given">Ortwin</namePart><namePart type="family">Rott</namePart><affiliation>INSERM U. 283, Hôpital Cochin, Université René Descartes, 27 rue du Fg. St.-Jacques, F-75674, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal" displayLabel="corresp"><namePart type="given">Jeannine</namePart><namePart type="family">Charreire</namePart><affiliation>INSERM U. 283, Hôpital Cochin, Université René Descartes, 27 rue du Fg. St.-Jacques, F-75674, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Evelyne</namePart><namePart type="family">Cash</namePart><affiliation>INSERM U. 283, Hôpital Cochin, Université René Descartes, 27 rue du Fg. St.-Jacques, F-75674, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="OriginalPaper" 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>Springer-Verlag</publisher><place><placeTerm type="text">Berlin/Heidelberg</placeTerm></place><dateCreated encoding="w3cdtf">1995-10-03</dateCreated><dateIssued encoding="w3cdtf">1996-02-01</dateIssued><copyrightDate encoding="w3cdtf">1996</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><abstract lang="en">Abstract: Influenza A viruses display T cell-independent polyclonal B cell-activating properties which are mediated by the B cell-superstimulatory envelope glycoprotein hemagglutinin (HA). In this report, the receptor-binding requirements for B cell activation by influenza viruses were expected. Neuraminidase treatment of resting mature B cells from BALB/c mice abrogated late (proliferation/immunoglobulin synthesis), early (up-regulation of cell surface markers, including CD25, B220, and B7-1) and veryearly events (homotypic adhesion) in virus-responding B lymphocytes. Similarly, pretreatment of murine responder cells with different inhibitors ofN-glycosylation (tunicamycin, deoxymannojirimycin) significantly suppressed subsequent B lymphocyte activation by HA, but not control responses to lipopolysaccharide or anti-μ. Assays with chimeric HA transfectants, expressing the loop region of epitope B (amino acids 155–160) of the globular head of H2 (high B cell-stimulatory subtype) or H3 (medium-stimulatory subtype) on the protein backbone of a low-stimulatory subtype (H1) failed to alter the B cell-stimulatory activity of the virus, suggesting that the hypervariable loop region is not crucial in determining the B cell-activating properties of the protein. Collectively, our results imply that the B cell-superstimulatory function of influenza virus HA is not mediated by a direct protein/protein interaction, but via binding of HA to terminal sialic acid residues on cell surface receptor glycoproteins. These findings identify the influenza virus HA glycoprotein as the first viral lectin with lymphocyte-activating properties.</abstract><note>Original Investigation</note><subject lang="en"><genre>Key words</genre><topic>Influenza virus</topic><topic>Superantigen</topic><topic>B cell activation</topic></subject><relatedItem type="host"><titleInfo><title>Medical Microbiology and Immunology</title></titleInfo><titleInfo type="abbreviated"><title>Med Microbiol Immunol</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>Springer</publisher><dateIssued encoding="w3cdtf">1996-02-01</dateIssued><copyrightDate encoding="w3cdtf">1996</copyrightDate></originInfo><subject><genre>Biomedicine</genre><topic>Immunology</topic><topic>Medical Microbiology</topic></subject><identifier type="ISSN">0300-8584</identifier><identifier type="eISSN">1432-1831</identifier><identifier type="JournalID">430</identifier><identifier type="IssueArticleCount">7</identifier><identifier type="VolumeIssueCount">4</identifier><part><date>1996</date><detail type="volume"><number>184</number><caption>vol.</caption></detail><detail type="issue"><number>4</number><caption>no.</caption></detail><extent unit="pages"><start>185</start><end>193</end></extent></part><recordInfo><recordOrigin>Springer-Verlag, 1996</recordOrigin></recordInfo></relatedItem><identifier type="istex">D7310E89F1F62F7DF84F75B4B166EAA695634DE0</identifier><identifier type="ark">ark:/67375/1BB-RMF521W1-9</identifier><identifier type="DOI">10.1007/BF02456134</identifier><identifier type="ArticleID">BF02456134</identifier><identifier type="ArticleID">Art6</identifier><accessCondition type="use and reproduction" contentType="copyright">Springer-Verlag, 1996</accessCondition><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-3XSW68JL-F">springer</recordContentSource><recordOrigin>Springer-Verlag, 1996</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/1BB-RMF521W1-9/record.json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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