Mycobacterium tuberculosis programs mesenchymal stem cells to establish dormancy and persistence.
Identifieur interne : 000079 ( Main/Exploration ); précédent : 000078; suivant : 000080Mycobacterium tuberculosis programs mesenchymal stem cells to establish dormancy and persistence.
Auteurs : Samreen Fatima [Inde] ; Shashank Shivaji Kamble [Inde] ; Ved Prakash Dwivedi [Inde] ; Debapriya Bhattacharya [Inde] ; Santosh Kumar [Inde] ; Anand Ranganathan [Inde] ; Luc Van Kaer [États-Unis] ; Sujata Mohanty [Inde] ; Gobardhan Das [Inde]Source :
- The Journal of clinical investigation [ 1558-8238 ] ; 2020.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Cellules souches mésenchymateuses (anatomopathologie), Cellules souches mésenchymateuses (microbiologie), Cellules souches mésenchymateuses (métabolisme), Humains (MeSH), Lipides (biosynthèse), Modèles animaux de maladie humaine (MeSH), Mycobacterium tuberculosis (métabolisme), Mycobacterium tuberculosis (pathogénicité), Phagosomes (anatomopathologie), Phagosomes (microbiologie), Phagosomes (métabolisme), Reprogrammation cellulaire (MeSH), Souris (MeSH), Tuberculose (anatomopathologie), Tuberculose (métabolisme).
- MESH :
- anatomopathologie : Cellules souches mésenchymateuses, Phagosomes, Tuberculose.
- biosynthèse : Lipides.
- microbiologie : Cellules souches mésenchymateuses, Phagosomes.
- métabolisme : Cellules souches mésenchymateuses, Mycobacterium tuberculosis, Phagosomes, Tuberculose.
- pathogénicité : Mycobacterium tuberculosis.
- Animaux, Humains, Modèles animaux de maladie humaine, Reprogrammation cellulaire, Souris.
English descriptors
- KwdEn :
- Animals (MeSH), Autophagic Cell Death (MeSH), Cellular Reprogramming (MeSH), Disease Models, Animal (MeSH), Humans (MeSH), Lipids (biosynthesis), Mesenchymal Stem Cells (metabolism), Mesenchymal Stem Cells (microbiology), Mesenchymal Stem Cells (pathology), Mice (MeSH), Mycobacterium tuberculosis (metabolism), Mycobacterium tuberculosis (pathogenicity), Phagosomes (metabolism), Phagosomes (microbiology), Phagosomes (pathology), Tuberculosis (metabolism), Tuberculosis (pathology).
- MESH :
- chemical , biosynthesis : Lipids.
- metabolism : Mesenchymal Stem Cells, Mycobacterium tuberculosis, Phagosomes, Tuberculosis.
- microbiology : Mesenchymal Stem Cells, Phagosomes.
- pathogenicity : Mycobacterium tuberculosis.
- pathology : Mesenchymal Stem Cells, Phagosomes, Tuberculosis.
- Animals, Autophagic Cell Death, Cellular Reprogramming, Disease Models, Animal, Humans, Mice.
Abstract
Tuberculosis (TB) remains a major infectious disease worldwide. TB treatment displays a biphasic bacterial clearance, in which the majority of bacteria clear within the first month of treatment, but residual bacteria remain nonresponsive to treatment and eventually may become resistant. Here, we have shown that Mycobacterium tuberculosis was taken up by mesenchymal stem cells (MSCs), where it established dormancy and became highly nonresponsive to isoniazid, a major constituent of directly observed treatment short course (DOTS). Dormant M. tuberculosis induced quiescence in MSCs and promoted their long-term survival. Unlike macrophages, where M. tuberculosis resides in early-phagosomal compartments, in MSCs the majority of bacilli were found in the cytosol, where they promoted rapid lipid synthesis, hiding within lipid droplets. Inhibition of lipid synthesis prevented dormancy and sensitized the organisms to isoniazid. Thus, we have established that M. tuberculosis gains dormancy in MSCs, which serve as a long-term natural reservoir of dormant M. tuberculosis. Interestingly, in the murine model of TB, induction of autophagy eliminated M. tuberculosis from MSCs, and consequently, the addition of rapamycin to an isoniazid treatment regimen successfully attained sterile clearance and prevented disease reactivation.
DOI: 10.1172/JCI128043
PubMed: 31647784
PubMed Central: PMC6994115
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Fatima</name><affiliation wicri:level="1"><nlm:affiliation>Special Centre for Molecular Medicine, Jawaharlal Nehru University, New Delhi, India.</nlm:affiliation><country xml:lang="fr">Inde</country><wicri:regionArea>Special Centre for Molecular Medicine, Jawaharlal Nehru University, New Delhi</wicri:regionArea><wicri:noRegion>New Delhi</wicri:noRegion></affiliation></author><author><name sortKey="Kamble, Shashank Shivaji" sort="Kamble, Shashank Shivaji" uniqKey="Kamble S" first="Shashank Shivaji" last="Kamble">Shashank Shivaji Kamble</name><affiliation wicri:level="1"><nlm:affiliation>Special Centre for Molecular Medicine, Jawaharlal Nehru University, New Delhi, India.</nlm:affiliation><country xml:lang="fr">Inde</country><wicri:regionArea>Special Centre for Molecular Medicine, Jawaharlal Nehru University, New Delhi</wicri:regionArea><wicri:noRegion>New Delhi</wicri:noRegion></affiliation></author><author><name sortKey="Dwivedi, Ved Prakash" sort="Dwivedi, Ved Prakash" uniqKey="Dwivedi V" first="Ved Prakash" last="Dwivedi">Ved Prakash Dwivedi</name><affiliation wicri:level="1"><nlm:affiliation>International Centre for Genetic Engineering and Biotechnology, New Delhi, India.</nlm:affiliation><country xml:lang="fr">Inde</country><wicri:regionArea>International Centre for Genetic Engineering and Biotechnology, New Delhi</wicri:regionArea><wicri:noRegion>New Delhi</wicri:noRegion></affiliation></author><author><name sortKey="Bhattacharya, Debapriya" sort="Bhattacharya, Debapriya" uniqKey="Bhattacharya D" first="Debapriya" last="Bhattacharya">Debapriya Bhattacharya</name><affiliation wicri:level="1"><nlm:affiliation>Special Centre for Molecular Medicine, Jawaharlal Nehru University, New Delhi, India.</nlm:affiliation><country xml:lang="fr">Inde</country><wicri:regionArea>Special Centre for Molecular Medicine, Jawaharlal Nehru University, New Delhi</wicri:regionArea><wicri:noRegion>New Delhi</wicri:noRegion></affiliation><affiliation 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Ranganathan</name><affiliation wicri:level="1"><nlm:affiliation>Special Centre for Molecular Medicine, Jawaharlal Nehru University, New Delhi, India.</nlm:affiliation><country xml:lang="fr">Inde</country><wicri:regionArea>Special Centre for Molecular Medicine, Jawaharlal Nehru University, New Delhi</wicri:regionArea><wicri:noRegion>New Delhi</wicri:noRegion></affiliation></author><author><name sortKey="Van Kaer, Luc" sort="Van Kaer, Luc" uniqKey="Van Kaer L" first="Luc" last="Van Kaer">Luc Van Kaer</name><affiliation wicri:level="2"><nlm:affiliation>Department of Pathology, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pathology, Vanderbilt University School of Medicine, Nashville, Tennessee</wicri:regionArea><placeName><region type="state">Tennessee</region></placeName></affiliation></author><author><name sortKey="Mohanty, Sujata" sort="Mohanty, Sujata" uniqKey="Mohanty S" first="Sujata" last="Mohanty">Sujata Mohanty</name><affiliation wicri:level="1"><nlm:affiliation>All India Institute of Medical Sciences, New Delhi, India.</nlm:affiliation><country xml:lang="fr">Inde</country><wicri:regionArea>All India Institute of Medical Sciences, New Delhi</wicri:regionArea><wicri:noRegion>New Delhi</wicri:noRegion></affiliation></author><author><name sortKey="Das, Gobardhan" sort="Das, Gobardhan" uniqKey="Das G" first="Gobardhan" last="Das">Gobardhan Das</name><affiliation wicri:level="1"><nlm:affiliation>Special Centre for Molecular Medicine, Jawaharlal Nehru University, New Delhi, India.</nlm:affiliation><country xml:lang="fr">Inde</country><wicri:regionArea>Special Centre for Molecular Medicine, Jawaharlal Nehru University, New Delhi</wicri:regionArea><wicri:noRegion>New Delhi</wicri:noRegion></affiliation></author></analytic><series><title level="j">The Journal of clinical investigation</title><idno type="eISSN">1558-8238</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Autophagic Cell Death (MeSH)</term><term>Cellular Reprogramming (MeSH)</term><term>Disease Models, Animal (MeSH)</term><term>Humans (MeSH)</term><term>Lipids (biosynthesis)</term><term>Mesenchymal Stem Cells (metabolism)</term><term>Mesenchymal Stem Cells (microbiology)</term><term>Mesenchymal Stem Cells (pathology)</term><term>Mice (MeSH)</term><term>Mycobacterium tuberculosis (metabolism)</term><term>Mycobacterium tuberculosis (pathogenicity)</term><term>Phagosomes (metabolism)</term><term>Phagosomes (microbiology)</term><term>Phagosomes (pathology)</term><term>Tuberculosis (metabolism)</term><term>Tuberculosis (pathology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term><term>Cellules souches mésenchymateuses (anatomopathologie)</term><term>Cellules souches mésenchymateuses (microbiologie)</term><term>Cellules souches mésenchymateuses (métabolisme)</term><term>Humains (MeSH)</term><term>Lipides (biosynthèse)</term><term>Modèles animaux de maladie humaine (MeSH)</term><term>Mycobacterium tuberculosis (métabolisme)</term><term>Mycobacterium tuberculosis (pathogénicité)</term><term>Phagosomes (anatomopathologie)</term><term>Phagosomes (microbiologie)</term><term>Phagosomes (métabolisme)</term><term>Reprogrammation cellulaire (MeSH)</term><term>Souris (MeSH)</term><term>Tuberculose (anatomopathologie)</term><term>Tuberculose (métabolisme)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Lipids</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Cellules souches mésenchymateuses</term><term>Phagosomes</term><term>Tuberculose</term></keywords><keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Lipides</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Mesenchymal Stem Cells</term><term>Mycobacterium tuberculosis</term><term>Phagosomes</term><term>Tuberculosis</term></keywords><keywords scheme="MESH" qualifier="microbiologie" xml:lang="fr"><term>Cellules souches mésenchymateuses</term><term>Phagosomes</term></keywords><keywords scheme="MESH" qualifier="microbiology" xml:lang="en"><term>Mesenchymal Stem Cells</term><term>Phagosomes</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cellules souches mésenchymateuses</term><term>Mycobacterium tuberculosis</term><term>Phagosomes</term><term>Tuberculose</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Mycobacterium tuberculosis</term></keywords><keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Mycobacterium tuberculosis</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Mesenchymal Stem Cells</term><term>Phagosomes</term><term>Tuberculosis</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Autophagic Cell Death</term><term>Cellular Reprogramming</term><term>Disease Models, Animal</term><term>Humans</term><term>Mice</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Humains</term><term>Modèles animaux de maladie humaine</term><term>Reprogrammation cellulaire</term><term>Souris</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Tuberculosis (TB) remains a major infectious disease worldwide. TB treatment displays a biphasic bacterial clearance, in which the majority of bacteria clear within the first month of treatment, but residual bacteria remain nonresponsive to treatment and eventually may become resistant. Here, we have shown that Mycobacterium tuberculosis was taken up by mesenchymal stem cells (MSCs), where it established dormancy and became highly nonresponsive to isoniazid, a major constituent of directly observed treatment short course (DOTS). Dormant M. tuberculosis induced quiescence in MSCs and promoted their long-term survival. Unlike macrophages, where M. tuberculosis resides in early-phagosomal compartments, in MSCs the majority of bacilli were found in the cytosol, where they promoted rapid lipid synthesis, hiding within lipid droplets. Inhibition of lipid synthesis prevented dormancy and sensitized the organisms to isoniazid. Thus, we have established that M. tuberculosis gains dormancy in MSCs, which serve as a long-term natural reservoir of dormant M. tuberculosis. Interestingly, in the murine model of TB, induction of autophagy eliminated M. tuberculosis from MSCs, and consequently, the addition of rapamycin to an isoniazid treatment regimen successfully attained sterile clearance and prevented disease reactivation.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">31647784</PMID><DateCompleted><Year>2020</Year><Month>09</Month><Day>14</Day></DateCompleted><DateRevised><Year>2020</Year><Month>09</Month><Day>14</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1558-8238</ISSN><JournalIssue CitedMedium="Internet"><Volume>130</Volume><Issue>2</Issue><PubDate><Year>2020</Year><Month>02</Month><Day>03</Day></PubDate></JournalIssue><Title>The Journal of clinical investigation</Title><ISOAbbreviation>J Clin Invest</ISOAbbreviation></Journal><ArticleTitle>Mycobacterium tuberculosis programs mesenchymal stem cells to establish dormancy and persistence.</ArticleTitle><Pagination><MedlinePgn>655-661</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1172/JCI128043</ELocationID><ELocationID EIdType="pii" ValidYN="Y">128043</ELocationID><Abstract><AbstractText>Tuberculosis (TB) remains a major infectious disease worldwide. TB treatment displays a biphasic bacterial clearance, in which the majority of bacteria clear within the first month of treatment, but residual bacteria remain nonresponsive to treatment and eventually may become resistant. Here, we have shown that Mycobacterium tuberculosis was taken up by mesenchymal stem cells (MSCs), where it established dormancy and became highly nonresponsive to isoniazid, a major constituent of directly observed treatment short course (DOTS). Dormant M. tuberculosis induced quiescence in MSCs and promoted their long-term survival. Unlike macrophages, where M. tuberculosis resides in early-phagosomal compartments, in MSCs the majority of bacilli were found in the cytosol, where they promoted rapid lipid synthesis, hiding within lipid droplets. Inhibition of lipid synthesis prevented dormancy and sensitized the organisms to isoniazid. Thus, we have established that M. tuberculosis gains dormancy in MSCs, which serve as a long-term natural reservoir of dormant M. tuberculosis. Interestingly, in the murine model of TB, induction of autophagy eliminated M. tuberculosis from MSCs, and consequently, the addition of rapamycin to an isoniazid treatment regimen successfully attained sterile clearance and prevented disease reactivation.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Fatima</LastName><ForeName>Samreen</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Special Centre for Molecular Medicine, Jawaharlal Nehru University, New Delhi, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kamble</LastName><ForeName>Shashank Shivaji</ForeName><Initials>SS</Initials><AffiliationInfo><Affiliation>Special Centre for Molecular Medicine, Jawaharlal Nehru University, New Delhi, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dwivedi</LastName><ForeName>Ved Prakash</ForeName><Initials>VP</Initials><AffiliationInfo><Affiliation>International Centre for Genetic Engineering and Biotechnology, New Delhi, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bhattacharya</LastName><ForeName>Debapriya</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Special Centre for Molecular Medicine, Jawaharlal Nehru University, New Delhi, India.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Centre for Biotechnology, Siksha 'O' Anusandhan Deemed University, Bhubaneswar, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kumar</LastName><ForeName>Santosh</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>International Centre for Genetic Engineering and Biotechnology, New Delhi, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ranganathan</LastName><ForeName>Anand</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Special Centre for Molecular Medicine, Jawaharlal Nehru University, New Delhi, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Van Kaer</LastName><ForeName>Luc</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Pathology, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mohanty</LastName><ForeName>Sujata</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>All India Institute of Medical Sciences, New Delhi, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Das</LastName><ForeName>Gobardhan</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Special Centre for Molecular Medicine, Jawaharlal Nehru University, New Delhi, India.</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></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Clin Invest</MedlineTA><NlmUniqueID>7802877</NlmUniqueID><ISSNLinking>0021-9738</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008055">Lipids</NameOfSubstance></Chemical></ChemicalList><CitationSubset>AIM</CitationSubset><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000080549" MajorTopicYN="Y">Autophagic Cell Death</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D065150" MajorTopicYN="Y">Cellular Reprogramming</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008055" MajorTopicYN="N">Lipids</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="N">biosynthesis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D059630" MajorTopicYN="Y">Mesenchymal Stem Cells</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009169" MajorTopicYN="Y">Mycobacterium tuberculosis</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000472" MajorTopicYN="N">pathogenicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010588" MajorTopicYN="N">Phagosomes</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014376" MajorTopicYN="Y">Tuberculosis</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Autophagy</Keyword><Keyword MajorTopicYN="Y">Bacterial infections</Keyword><Keyword MajorTopicYN="Y">Infectious disease</Keyword><Keyword MajorTopicYN="Y">Stem cells</Keyword><Keyword MajorTopicYN="Y">Tuberculosis</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2019</Year><Month>02</Month><Day>08</Day></PubMedPubDate><PubMedPubDate 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IdType="pubmed">19349380</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></pubmed><affiliations><list><country><li>Inde</li><li>États-Unis</li></country><region><li>Tennessee</li></region></list><tree><country name="Inde"><noRegion><name sortKey="Fatima, Samreen" sort="Fatima, Samreen" uniqKey="Fatima S" first="Samreen" last="Fatima">Samreen Fatima</name></noRegion><name sortKey="Bhattacharya, Debapriya" sort="Bhattacharya, Debapriya" uniqKey="Bhattacharya D" first="Debapriya" last="Bhattacharya">Debapriya Bhattacharya</name><name sortKey="Bhattacharya, Debapriya" sort="Bhattacharya, Debapriya" uniqKey="Bhattacharya D" first="Debapriya" last="Bhattacharya">Debapriya Bhattacharya</name><name sortKey="Das, Gobardhan" sort="Das, Gobardhan" uniqKey="Das G" first="Gobardhan" last="Das">Gobardhan Das</name><name sortKey="Dwivedi, Ved Prakash" sort="Dwivedi, Ved Prakash" uniqKey="Dwivedi V" first="Ved Prakash" last="Dwivedi">Ved Prakash Dwivedi</name><name sortKey="Kamble, Shashank Shivaji" sort="Kamble, Shashank Shivaji" uniqKey="Kamble S" first="Shashank Shivaji" last="Kamble">Shashank Shivaji Kamble</name><name sortKey="Kumar, Santosh" sort="Kumar, Santosh" uniqKey="Kumar S" first="Santosh" last="Kumar">Santosh Kumar</name><name sortKey="Mohanty, Sujata" sort="Mohanty, Sujata" uniqKey="Mohanty S" first="Sujata" last="Mohanty">Sujata Mohanty</name><name sortKey="Ranganathan, Anand" sort="Ranganathan, Anand" uniqKey="Ranganathan A" first="Anand" last="Ranganathan">Anand Ranganathan</name></country><country name="États-Unis"><region name="Tennessee"><name sortKey="Van Kaer, Luc" sort="Van Kaer, Luc" uniqKey="Van Kaer L" first="Luc" last="Van Kaer">Luc Van Kaer</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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