Induction of B7-H1 receptor by bacterial cells fractions of Porphyromonas gingivalis on human oral epithelial cells: B7-H1 induction by Porphyromonas gingivalis fractions.
Identifieur interne : 000116 ( Main/Exploration ); précédent : 000115; suivant : 000117Induction of B7-H1 receptor by bacterial cells fractions of Porphyromonas gingivalis on human oral epithelial cells: B7-H1 induction by Porphyromonas gingivalis fractions.
Auteurs : S. Groeger [Allemagne] ; F. Jarzina [Allemagne] ; U. Mamat [Allemagne] ; J. Meyle [Allemagne]Source :
- Immunobiology [ 1878-3279 ] ; 2017.
Descripteurs français
- KwdFr :
- ARN messager (génétique), ARN messager (métabolisme), Antigène CD274 (génétique), Antigène CD274 (métabolisme), Cellules cultivées (MeSH), Cellules épithéliales (effets des médicaments et des substances chimiques), Cellules épithéliales (microbiologie), Cellules épithéliales (métabolisme), Expression des gènes (MeSH), Humains (MeSH), Infections à Bacteroidaceae (génétique), Infections à Bacteroidaceae (immunologie), Infections à Bacteroidaceae (microbiologie), Infections à Bacteroidaceae (métabolisme), Interféron gamma (métabolisme), Interféron gamma (pharmacologie), Kératinocytes (immunologie), Kératinocytes (microbiologie), Kératinocytes (métabolisme), Lignée cellulaire (MeSH), Muqueuse de la bouche (immunologie), Muqueuse de la bouche (microbiologie), Muqueuse de la bouche (métabolisme), Porphyromonas gingivalis (immunologie).
- MESH :
- effets des médicaments et des substances chimiques : Cellules épithéliales.
- génétique : ARN messager, Antigène CD274, Infections à Bacteroidaceae.
- immunologie : Infections à Bacteroidaceae, Kératinocytes, Muqueuse de la bouche, Porphyromonas gingivalis.
- microbiologie : Cellules épithéliales, Infections à Bacteroidaceae, Kératinocytes, Muqueuse de la bouche.
- métabolisme : ARN messager, Antigène CD274, Cellules épithéliales, Infections à Bacteroidaceae, Interféron gamma, Kératinocytes, Muqueuse de la bouche.
- pharmacologie : Interféron gamma.
- Cellules cultivées, Expression des gènes, Humains, Lignée cellulaire.
English descriptors
- KwdEn :
- B7-H1 Antigen (genetics), B7-H1 Antigen (metabolism), Bacteroidaceae Infections (genetics), Bacteroidaceae Infections (immunology), Bacteroidaceae Infections (metabolism), Bacteroidaceae Infections (microbiology), Cell Line (MeSH), Cells, Cultured (MeSH), Epithelial Cells (drug effects), Epithelial Cells (metabolism), Epithelial Cells (microbiology), Gene Expression (MeSH), Humans (MeSH), Interferon-gamma (metabolism), Interferon-gamma (pharmacology), Keratinocytes (immunology), Keratinocytes (metabolism), Keratinocytes (microbiology), Mouth Mucosa (immunology), Mouth Mucosa (metabolism), Mouth Mucosa (microbiology), Porphyromonas gingivalis (immunology), RNA, Messenger (genetics), RNA, Messenger (metabolism).
- MESH :
- chemical , genetics : B7-H1 Antigen, RNA, Messenger.
- chemical , metabolism : B7-H1 Antigen, Interferon-gamma, RNA, Messenger.
- drug effects : Epithelial Cells.
- genetics : Bacteroidaceae Infections.
- immunology : Bacteroidaceae Infections, Keratinocytes, Mouth Mucosa, Porphyromonas gingivalis.
- metabolism : Bacteroidaceae Infections, Epithelial Cells, Keratinocytes, Mouth Mucosa.
- microbiology : Bacteroidaceae Infections, Epithelial Cells, Keratinocytes, Mouth Mucosa.
- chemical , pharmacology : Interferon-gamma.
- Cell Line, Cells, Cultured, Gene Expression, Humans.
Abstract
The immune-regulatory B7-H1 receptor, also known as programmed death-ligand 1 (PD-L1), plays an important role in cell-mediated immune response. It is a co-signaling molecule that mediates regulation of T cell activation and tolerance and is able to negatively regulate activated T cell functions and survival. High expression of B7-H1 in host cells may contribute to the chronicity of inflammatory disorders and represents a possible mechanism of immune evasion. Porphyromonas gingivalis is regarded as a keystone pathogen in periodontitis and is able to invade host cells and disposes a variety of virulence factors including lipopolysaccharide (LPS), fimbriae and proteases such as gingipains. Based on previous studies that demonstrated the capability of P. gingivalis to induce up-regulation of PD-L1 in malignant and non-malignant oral epithelial cells, the aim of the present work was to analyse the potential of various cellular components of P. gingivalis to induce the PD-L1 receptor. Human squamous carcinoma cells and primary gingival keratinocytes were stimulated with total, inner and outer membrane fractions, cytosolic proteins, as well as LPS and peptidoglycans. PD-L1 protein expression was investigated by Western blot analysis and RT-PCR. It was demonstrated that the total membrane fraction induced the highest up-regulation in B7-H1 expression, followed by the outer and inner membrane, whereas cytosolic proteins and LPS did not. In conclusion, we provide evidence that the membrane fraction of P. gingivalis is responsible for up-regulation of the immune-regulatory receptor PD-L1 in squamous carcinoma cells and gingival keratinocytes, and thus may support immune evasion of oral carcinomas.
DOI: 10.1016/j.imbio.2016.10.011
PubMed: 28164807
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Groeger</name><affiliation wicri:level="1"><nlm:affiliation>Department of Periodontology, Justus-Liebig-University of Giessen, Germany. Electronic address: Sabine.E.Groeger@dentist.med.uni-giessen.de.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Periodontology, Justus-Liebig-University of Giessen</wicri:regionArea><wicri:noRegion>Justus-Liebig-University of Giessen</wicri:noRegion><wicri:noRegion>Justus-Liebig-University of Giessen</wicri:noRegion><wicri:noRegion>Justus-Liebig-University of Giessen</wicri:noRegion></affiliation></author><author><name sortKey="Jarzina, F" sort="Jarzina, F" uniqKey="Jarzina F" first="F" last="Jarzina">F. 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Mamat</name><affiliation wicri:level="1"><nlm:affiliation>Division of Structural Biochemistry, Research Center Borstel, Leibniz-Center for Medicine and Bioscience, Borstel, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Division of Structural Biochemistry, Research Center Borstel, Leibniz-Center for Medicine and Bioscience, Borstel</wicri:regionArea><wicri:noRegion>Borstel</wicri:noRegion><wicri:noRegion>Borstel</wicri:noRegion><wicri:noRegion>Borstel</wicri:noRegion></affiliation></author><author><name sortKey="Meyle, J" sort="Meyle, J" uniqKey="Meyle J" first="J" last="Meyle">J. Meyle</name><affiliation wicri:level="1"><nlm:affiliation>Department of Periodontology, Justus-Liebig-University of Giessen, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Periodontology, Justus-Liebig-University of Giessen</wicri:regionArea><wicri:noRegion>Justus-Liebig-University of Giessen</wicri:noRegion><wicri:noRegion>Justus-Liebig-University of Giessen</wicri:noRegion><wicri:noRegion>Justus-Liebig-University of Giessen</wicri:noRegion></affiliation></author></analytic><series><title level="j">Immunobiology</title><idno type="eISSN">1878-3279</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>B7-H1 Antigen (genetics)</term><term>B7-H1 Antigen (metabolism)</term><term>Bacteroidaceae Infections (genetics)</term><term>Bacteroidaceae Infections (immunology)</term><term>Bacteroidaceae Infections (metabolism)</term><term>Bacteroidaceae Infections (microbiology)</term><term>Cell Line (MeSH)</term><term>Cells, Cultured (MeSH)</term><term>Epithelial Cells (drug effects)</term><term>Epithelial Cells (metabolism)</term><term>Epithelial Cells (microbiology)</term><term>Gene Expression (MeSH)</term><term>Humans (MeSH)</term><term>Interferon-gamma (metabolism)</term><term>Interferon-gamma (pharmacology)</term><term>Keratinocytes (immunology)</term><term>Keratinocytes (metabolism)</term><term>Keratinocytes (microbiology)</term><term>Mouth Mucosa (immunology)</term><term>Mouth Mucosa (metabolism)</term><term>Mouth Mucosa (microbiology)</term><term>Porphyromonas gingivalis (immunology)</term><term>RNA, Messenger (genetics)</term><term>RNA, Messenger (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>ARN messager (génétique)</term><term>ARN messager (métabolisme)</term><term>Antigène CD274 (génétique)</term><term>Antigène CD274 (métabolisme)</term><term>Cellules cultivées (MeSH)</term><term>Cellules épithéliales (effets des médicaments et des substances chimiques)</term><term>Cellules épithéliales (microbiologie)</term><term>Cellules épithéliales (métabolisme)</term><term>Expression des gènes (MeSH)</term><term>Humains (MeSH)</term><term>Infections à Bacteroidaceae (génétique)</term><term>Infections à Bacteroidaceae (immunologie)</term><term>Infections à Bacteroidaceae (microbiologie)</term><term>Infections à Bacteroidaceae (métabolisme)</term><term>Interféron gamma (métabolisme)</term><term>Interféron gamma (pharmacologie)</term><term>Kératinocytes (immunologie)</term><term>Kératinocytes (microbiologie)</term><term>Kératinocytes (métabolisme)</term><term>Lignée cellulaire (MeSH)</term><term>Muqueuse de la bouche (immunologie)</term><term>Muqueuse de la bouche (microbiologie)</term><term>Muqueuse de la bouche (métabolisme)</term><term>Porphyromonas gingivalis (immunologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>B7-H1 Antigen</term><term>RNA, Messenger</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>B7-H1 Antigen</term><term>Interferon-gamma</term><term>RNA, Messenger</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Epithelial Cells</term></keywords><keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Cellules épithéliales</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Bacteroidaceae Infections</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>ARN messager</term><term>Antigène CD274</term><term>Infections à Bacteroidaceae</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Infections à Bacteroidaceae</term><term>Kératinocytes</term><term>Muqueuse de la bouche</term><term>Porphyromonas gingivalis</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Bacteroidaceae Infections</term><term>Keratinocytes</term><term>Mouth Mucosa</term><term>Porphyromonas gingivalis</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Bacteroidaceae Infections</term><term>Epithelial Cells</term><term>Keratinocytes</term><term>Mouth Mucosa</term></keywords><keywords scheme="MESH" qualifier="microbiologie" xml:lang="fr"><term>Cellules épithéliales</term><term>Infections à Bacteroidaceae</term><term>Kératinocytes</term><term>Muqueuse de la bouche</term></keywords><keywords scheme="MESH" qualifier="microbiology" xml:lang="en"><term>Bacteroidaceae Infections</term><term>Epithelial Cells</term><term>Keratinocytes</term><term>Mouth Mucosa</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>ARN messager</term><term>Antigène CD274</term><term>Cellules épithéliales</term><term>Infections à Bacteroidaceae</term><term>Interféron gamma</term><term>Kératinocytes</term><term>Muqueuse de la bouche</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Interféron gamma</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Interferon-gamma</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Line</term><term>Cells, Cultured</term><term>Gene Expression</term><term>Humans</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Cellules cultivées</term><term>Expression des gènes</term><term>Humains</term><term>Lignée cellulaire</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The immune-regulatory B7-H1 receptor, also known as programmed death-ligand 1 (PD-L1), plays an important role in cell-mediated immune response. It is a co-signaling molecule that mediates regulation of T cell activation and tolerance and is able to negatively regulate activated T cell functions and survival. High expression of B7-H1 in host cells may contribute to the chronicity of inflammatory disorders and represents a possible mechanism of immune evasion. Porphyromonas gingivalis is regarded as a keystone pathogen in periodontitis and is able to invade host cells and disposes a variety of virulence factors including lipopolysaccharide (LPS), fimbriae and proteases such as gingipains. Based on previous studies that demonstrated the capability of P. gingivalis to induce up-regulation of PD-L1 in malignant and non-malignant oral epithelial cells, the aim of the present work was to analyse the potential of various cellular components of P. gingivalis to induce the PD-L1 receptor. Human squamous carcinoma cells and primary gingival keratinocytes were stimulated with total, inner and outer membrane fractions, cytosolic proteins, as well as LPS and peptidoglycans. PD-L1 protein expression was investigated by Western blot analysis and RT-PCR. It was demonstrated that the total membrane fraction induced the highest up-regulation in B7-H1 expression, followed by the outer and inner membrane, whereas cytosolic proteins and LPS did not. In conclusion, we provide evidence that the membrane fraction of P. gingivalis is responsible for up-regulation of the immune-regulatory receptor PD-L1 in squamous carcinoma cells and gingival keratinocytes, and thus may support immune evasion of oral carcinomas.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">28164807</PMID><DateCompleted><Year>2017</Year><Month>12</Month><Day>07</Day></DateCompleted><DateRevised><Year>2018</Year><Month>01</Month><Day>25</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1878-3279</ISSN><JournalIssue CitedMedium="Internet"><Volume>222</Volume><Issue>2</Issue><PubDate><Year>2017</Year><Month>02</Month></PubDate></JournalIssue><Title>Immunobiology</Title><ISOAbbreviation>Immunobiology</ISOAbbreviation></Journal><ArticleTitle>Induction of B7-H1 receptor by bacterial cells fractions of Porphyromonas gingivalis on human oral epithelial cells: B7-H1 induction by Porphyromonas gingivalis fractions.</ArticleTitle><Pagination><MedlinePgn>137-147</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0171-2985(16)30418-1</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.imbio.2016.10.011</ELocationID><Abstract><AbstractText>The immune-regulatory B7-H1 receptor, also known as programmed death-ligand 1 (PD-L1), plays an important role in cell-mediated immune response. It is a co-signaling molecule that mediates regulation of T cell activation and tolerance and is able to negatively regulate activated T cell functions and survival. High expression of B7-H1 in host cells may contribute to the chronicity of inflammatory disorders and represents a possible mechanism of immune evasion. Porphyromonas gingivalis is regarded as a keystone pathogen in periodontitis and is able to invade host cells and disposes a variety of virulence factors including lipopolysaccharide (LPS), fimbriae and proteases such as gingipains. Based on previous studies that demonstrated the capability of P. gingivalis to induce up-regulation of PD-L1 in malignant and non-malignant oral epithelial cells, the aim of the present work was to analyse the potential of various cellular components of P. gingivalis to induce the PD-L1 receptor. Human squamous carcinoma cells and primary gingival keratinocytes were stimulated with total, inner and outer membrane fractions, cytosolic proteins, as well as LPS and peptidoglycans. PD-L1 protein expression was investigated by Western blot analysis and RT-PCR. It was demonstrated that the total membrane fraction induced the highest up-regulation in B7-H1 expression, followed by the outer and inner membrane, whereas cytosolic proteins and LPS did not. In conclusion, we provide evidence that the membrane fraction of P. gingivalis is responsible for up-regulation of the immune-regulatory receptor PD-L1 in squamous carcinoma cells and gingival keratinocytes, and thus may support immune evasion of oral carcinomas.</AbstractText><CopyrightInformation>Copyright © 2016 Elsevier GmbH. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Groeger</LastName><ForeName>S</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Periodontology, Justus-Liebig-University of Giessen, Germany. Electronic address: Sabine.E.Groeger@dentist.med.uni-giessen.de.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jarzina</LastName><ForeName>F</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Department of Periodontology, Justus-Liebig-University of Giessen, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mamat</LastName><ForeName>U</ForeName><Initials>U</Initials><AffiliationInfo><Affiliation>Division of Structural Biochemistry, Research Center Borstel, Leibniz-Center for Medicine and Bioscience, Borstel, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Meyle</LastName><ForeName>J</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Periodontology, Justus-Liebig-University of Giessen, Germany.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>10</Month><Day>17</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Immunobiology</MedlineTA><NlmUniqueID>8002742</NlmUniqueID><ISSNLinking>0171-2985</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D060890">B7-H1 Antigen</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C423236">CD274 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D012333">RNA, Messenger</NameOfSubstance></Chemical><Chemical><RegistryNumber>82115-62-6</RegistryNumber><NameOfSubstance UI="D007371">Interferon-gamma</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D060890" MajorTopicYN="N">B7-H1 Antigen</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016866" MajorTopicYN="N">Bacteroidaceae Infections</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004847" MajorTopicYN="N">Epithelial Cells</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015870" MajorTopicYN="N">Gene Expression</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007371" MajorTopicYN="N">Interferon-gamma</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015603" MajorTopicYN="N">Keratinocytes</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009061" MajorTopicYN="N">Mouth Mucosa</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016966" MajorTopicYN="N">Porphyromonas gingivalis</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012333" MajorTopicYN="N">RNA, Messenger</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">B7-H1</Keyword><Keyword MajorTopicYN="Y">Immune evasion</Keyword><Keyword MajorTopicYN="Y">Immune-regulatory receptor</Keyword><Keyword MajorTopicYN="Y">Porphyromonas gingivalis membrane</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2016</Year><Month>01</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2016</Year><Month>10</Month><Day>15</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2017</Year><Month>2</Month><Day>7</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2017</Year><Month>2</Month><Day>7</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>12</Month><Day>8</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">28164807</ArticleId><ArticleId IdType="pii">S0171-2985(16)30418-1</ArticleId><ArticleId IdType="doi">10.1016/j.imbio.2016.10.011</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Allemagne</li></country></list><tree><country name="Allemagne"><noRegion><name sortKey="Groeger, S" sort="Groeger, S" uniqKey="Groeger S" first="S" last="Groeger">S. Groeger</name></noRegion><name sortKey="Jarzina, F" sort="Jarzina, F" uniqKey="Jarzina F" first="F" last="Jarzina">F. Jarzina</name><name sortKey="Mamat, U" sort="Mamat, U" uniqKey="Mamat U" first="U" last="Mamat">U. Mamat</name><name sortKey="Meyle, J" sort="Meyle, J" uniqKey="Meyle J" first="J" last="Meyle">J. Meyle</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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