IFN-γ regulates CD8+ memory T cell differentiation and survival in response to weak, but not strong, TCR signals.
Identifieur interne : 000C84 ( Main/Exploration ); précédent : 000C83; suivant : 000C85IFN-γ regulates CD8+ memory T cell differentiation and survival in response to weak, but not strong, TCR signals.
Auteurs : Diana Stoycheva [Allemagne] ; Katrin Deiser [Allemagne] ; Lilian St Rck [Allemagne] ; Gopala Nishanth ; Dirk Schlüter ; Wolfgang Uckert [Allemagne] ; Thomas Schüler [Allemagne]Source :
- Journal of immunology (Baltimore, Md. : 1950) [ 1550-6606 ] ; 2015.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Différenciation cellulaire (génétique), Différenciation cellulaire (immunologie), Interféron gamma (génétique), Interféron gamma (immunologie), Lymphocytes T CD8+ (immunologie), Mémoire immunologique (physiologie), Protéines proto-oncogènes c-bcl-2 (génétique), Protéines proto-oncogènes c-bcl-2 (immunologie), Protéines à domaine boîte-T (génétique), Protéines à domaine boîte-T (immunologie), Récepteur interféron (génétique), Récepteur interféron (immunologie), Récepteurs aux antigènes des cellules T (génétique), Récepteurs aux antigènes des cellules T (immunologie), Souris (MeSH), Souris knockout (MeSH), Survie cellulaire (génétique), Survie cellulaire (immunologie), Sélectine L (génétique), Sélectine L (immunologie), Sérine-thréonine kinases TOR (génétique), Sérine-thréonine kinases TOR (métabolisme), Transduction du signal (génétique), Transduction du signal (immunologie).
- MESH :
- génétique : Différenciation cellulaire, Interféron gamma, Protéines proto-oncogènes c-bcl-2, Protéines à domaine boîte-T, Récepteur interféron, Récepteurs aux antigènes des cellules T, Survie cellulaire, Sélectine L, Sérine-thréonine kinases TOR, Transduction du signal.
- immunologie : Différenciation cellulaire, Interféron gamma, Lymphocytes T CD8+, Protéines proto-oncogènes c-bcl-2, Protéines à domaine boîte-T, Récepteur interféron, Récepteurs aux antigènes des cellules T, Survie cellulaire, Sélectine L, Transduction du signal.
- métabolisme : Sérine-thréonine kinases TOR.
- physiologie : Mémoire immunologique.
- Animaux, Souris, Souris knockout.
English descriptors
- KwdEn :
- Animals (MeSH), CD8-Positive T-Lymphocytes (immunology), Cell Differentiation (genetics), Cell Differentiation (immunology), Cell Survival (genetics), Cell Survival (immunology), Immunologic Memory (physiology), Interferon-gamma (genetics), Interferon-gamma (immunology), L-Selectin (genetics), L-Selectin (immunology), Mice (MeSH), Mice, Knockout (MeSH), Proto-Oncogene Proteins c-bcl-2 (genetics), Proto-Oncogene Proteins c-bcl-2 (immunology), Receptors, Antigen, T-Cell (genetics), Receptors, Antigen, T-Cell (immunology), Receptors, Interferon (genetics), Receptors, Interferon (immunology), Signal Transduction (genetics), Signal Transduction (immunology), T-Box Domain Proteins (genetics), T-Box Domain Proteins (immunology), TOR Serine-Threonine Kinases (genetics), TOR Serine-Threonine Kinases (metabolism).
- MESH :
- chemical , genetics : Interferon-gamma, L-Selectin, Proto-Oncogene Proteins c-bcl-2, Receptors, Antigen, T-Cell, Receptors, Interferon, T-Box Domain Proteins, TOR Serine-Threonine Kinases.
- genetics : Cell Differentiation, Cell Survival, Signal Transduction.
- immunology : CD8-Positive T-Lymphocytes, Cell Differentiation, Cell Survival, Interferon-gamma, L-Selectin, Proto-Oncogene Proteins c-bcl-2, Receptors, Antigen, T-Cell, Receptors, Interferon, Signal Transduction, T-Box Domain Proteins.
- chemical , metabolism : TOR Serine-Threonine Kinases.
- physiology : Immunologic Memory.
- Animals, Mice, Mice, Knockout.
Abstract
In response to primary Ag contact, naive mouse CD8(+) T cells undergo clonal expansion and differentiate into effector T cells. After pathogen clearance, most effector T cells die, and only a small number of memory T cell precursors (TMPs) survive to form a pool of long-lived memory T cells (TMs). Although high- and low-affinity CD8(+) T cell clones are recruited into the primary response, the TM pool consists mainly of high-affinity clones. It remains unclear whether the more efficient expansion of high-affinity clones and/or cell-intrinsic processes exclude low-affinity T cells from the TM pool. In this article, we show that the lack of IFN-γR signaling in CD8(+) T cells promotes TM formation in response to weak, but not strong, TCR agonists. The IFN-γ-sensitive accumulation of TMs correlates with reduced mammalian target of rapamycin activation and the accumulation of long-lived CD62L(hi)Bcl-2(hi)Eomes(hi) TMPs. Reconstitution of mammalian target of rapamycin or IFN-γR signaling is sufficient to block this process. Hence, our data suggest that IFN-γR signaling actively blocks the formation of TMPs responding to weak TCR agonists, thereby promoting the accumulation of high-affinity T cells finally dominating the TM pool.
DOI: 10.4049/jimmunol.1402058
PubMed: 25480562
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Berlin</wicri:regionArea><placeName><region type="land" nuts="3">Berlin</region><settlement type="city">Berlin</settlement></placeName></affiliation></author></analytic><series><title level="j">Journal of immunology (Baltimore, Md. : 1950)</title><idno type="eISSN">1550-6606</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>CD8-Positive T-Lymphocytes (immunology)</term><term>Cell Differentiation (genetics)</term><term>Cell Differentiation (immunology)</term><term>Cell Survival (genetics)</term><term>Cell Survival (immunology)</term><term>Immunologic Memory (physiology)</term><term>Interferon-gamma (genetics)</term><term>Interferon-gamma (immunology)</term><term>L-Selectin (genetics)</term><term>L-Selectin (immunology)</term><term>Mice (MeSH)</term><term>Mice, Knockout (MeSH)</term><term>Proto-Oncogene Proteins c-bcl-2 (genetics)</term><term>Proto-Oncogene Proteins c-bcl-2 (immunology)</term><term>Receptors, Antigen, T-Cell (genetics)</term><term>Receptors, Antigen, T-Cell (immunology)</term><term>Receptors, Interferon (genetics)</term><term>Receptors, Interferon (immunology)</term><term>Signal Transduction (genetics)</term><term>Signal Transduction (immunology)</term><term>T-Box Domain Proteins (genetics)</term><term>T-Box Domain Proteins (immunology)</term><term>TOR Serine-Threonine Kinases (genetics)</term><term>TOR Serine-Threonine Kinases (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term><term>Différenciation cellulaire (génétique)</term><term>Différenciation cellulaire (immunologie)</term><term>Interféron gamma (génétique)</term><term>Interféron gamma (immunologie)</term><term>Lymphocytes T CD8+ (immunologie)</term><term>Mémoire immunologique (physiologie)</term><term>Protéines proto-oncogènes c-bcl-2 (génétique)</term><term>Protéines proto-oncogènes c-bcl-2 (immunologie)</term><term>Protéines à domaine boîte-T (génétique)</term><term>Protéines à domaine boîte-T (immunologie)</term><term>Récepteur interféron (génétique)</term><term>Récepteur interféron (immunologie)</term><term>Récepteurs aux antigènes des cellules T (génétique)</term><term>Récepteurs aux antigènes des cellules T (immunologie)</term><term>Souris (MeSH)</term><term>Souris knockout (MeSH)</term><term>Survie cellulaire (génétique)</term><term>Survie cellulaire (immunologie)</term><term>Sélectine L (génétique)</term><term>Sélectine L (immunologie)</term><term>Sérine-thréonine kinases TOR (génétique)</term><term>Sérine-thréonine kinases TOR (métabolisme)</term><term>Transduction du signal (génétique)</term><term>Transduction du signal (immunologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Interferon-gamma</term><term>L-Selectin</term><term>Proto-Oncogene Proteins c-bcl-2</term><term>Receptors, Antigen, T-Cell</term><term>Receptors, Interferon</term><term>T-Box Domain Proteins</term><term>TOR Serine-Threonine Kinases</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Cell Differentiation</term><term>Cell Survival</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Différenciation cellulaire</term><term>Interféron gamma</term><term>Protéines proto-oncogènes c-bcl-2</term><term>Protéines à domaine boîte-T</term><term>Récepteur interféron</term><term>Récepteurs aux antigènes des cellules T</term><term>Survie cellulaire</term><term>Sélectine L</term><term>Sérine-thréonine kinases TOR</term><term>Transduction du signal</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Différenciation cellulaire</term><term>Interféron gamma</term><term>Lymphocytes T CD8+</term><term>Protéines proto-oncogènes c-bcl-2</term><term>Protéines à domaine boîte-T</term><term>Récepteur interféron</term><term>Récepteurs aux antigènes des cellules T</term><term>Survie cellulaire</term><term>Sélectine L</term><term>Transduction du signal</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>CD8-Positive T-Lymphocytes</term><term>Cell Differentiation</term><term>Cell Survival</term><term>Interferon-gamma</term><term>L-Selectin</term><term>Proto-Oncogene Proteins c-bcl-2</term><term>Receptors, Antigen, T-Cell</term><term>Receptors, Interferon</term><term>Signal Transduction</term><term>T-Box Domain Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>TOR Serine-Threonine Kinases</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Sérine-thréonine kinases TOR</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Mémoire immunologique</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Immunologic Memory</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Mice</term><term>Mice, Knockout</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Souris</term><term>Souris knockout</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In response to primary Ag contact, naive mouse CD8(+) T cells undergo clonal expansion and differentiate into effector T cells. After pathogen clearance, most effector T cells die, and only a small number of memory T cell precursors (TMPs) survive to form a pool of long-lived memory T cells (TMs). Although high- and low-affinity CD8(+) T cell clones are recruited into the primary response, the TM pool consists mainly of high-affinity clones. It remains unclear whether the more efficient expansion of high-affinity clones and/or cell-intrinsic processes exclude low-affinity T cells from the TM pool. In this article, we show that the lack of IFN-γR signaling in CD8(+) T cells promotes TM formation in response to weak, but not strong, TCR agonists. The IFN-γ-sensitive accumulation of TMs correlates with reduced mammalian target of rapamycin activation and the accumulation of long-lived CD62L(hi)Bcl-2(hi)Eomes(hi) TMPs. Reconstitution of mammalian target of rapamycin or IFN-γR signaling is sufficient to block this process. Hence, our data suggest that IFN-γR signaling actively blocks the formation of TMPs responding to weak TCR agonists, thereby promoting the accumulation of high-affinity T cells finally dominating the TM pool. </div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25480562</PMID><DateCompleted><Year>2015</Year><Month>03</Month><Day>11</Day></DateCompleted><DateRevised><Year>2018</Year><Month>12</Month><Day>02</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1550-6606</ISSN><JournalIssue CitedMedium="Internet"><Volume>194</Volume><Issue>2</Issue><PubDate><Year>2015</Year><Month>Jan</Month><Day>15</Day></PubDate></JournalIssue><Title>Journal of immunology (Baltimore, Md. : 1950)</Title><ISOAbbreviation>J Immunol</ISOAbbreviation></Journal><ArticleTitle>IFN-γ regulates CD8+ memory T cell differentiation and survival in response to weak, but not strong, TCR signals.</ArticleTitle><Pagination><MedlinePgn>553-9</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.4049/jimmunol.1402058</ELocationID><Abstract><AbstractText>In response to primary Ag contact, naive mouse CD8(+) T cells undergo clonal expansion and differentiate into effector T cells. After pathogen clearance, most effector T cells die, and only a small number of memory T cell precursors (TMPs) survive to form a pool of long-lived memory T cells (TMs). Although high- and low-affinity CD8(+) T cell clones are recruited into the primary response, the TM pool consists mainly of high-affinity clones. It remains unclear whether the more efficient expansion of high-affinity clones and/or cell-intrinsic processes exclude low-affinity T cells from the TM pool. In this article, we show that the lack of IFN-γR signaling in CD8(+) T cells promotes TM formation in response to weak, but not strong, TCR agonists. The IFN-γ-sensitive accumulation of TMs correlates with reduced mammalian target of rapamycin activation and the accumulation of long-lived CD62L(hi)Bcl-2(hi)Eomes(hi) TMPs. Reconstitution of mammalian target of rapamycin or IFN-γR signaling is sufficient to block this process. Hence, our data suggest that IFN-γR signaling actively blocks the formation of TMPs responding to weak TCR agonists, thereby promoting the accumulation of high-affinity T cells finally dominating the TM pool. </AbstractText><CopyrightInformation>Copyright © 2015 by The American Association of Immunologists, Inc.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Stoycheva</LastName><ForeName>Diana</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Institute of Molecular and Clinical Immunology, Medical Faculty, Otto-von-Guericke University, 39120 Magdeburg, Germany; Institute of Immunology, Charité Berlin, 12200 Berlin, Germany;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Deiser</LastName><ForeName>Katrin</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Institute of Molecular and Clinical Immunology, Medical Faculty, Otto-von-Guericke University, 39120 Magdeburg, Germany; Institute of Immunology, Charité Berlin, 12200 Berlin, Germany;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Stärck</LastName><ForeName>Lilian</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Max-Delbrück-Center for Molecular Medicine, 13125 Berlin, Germany;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nishanth</LastName><ForeName>Gopala</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Institute of Medical Microbiology and Hospital Hygiene, Medical Faculty, Otto-von-Guericke University, 39120 Magdeburg, Germany; Organ-Specific Immune Regulation, Helmholtz Centre for Infection Research, 38124 Braunschweig, Germany; and.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Schlüter</LastName><ForeName>Dirk</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Institute of Medical Microbiology and Hospital Hygiene, Medical Faculty, Otto-von-Guericke University, 39120 Magdeburg, Germany; Organ-Specific Immune Regulation, Helmholtz Centre for Infection Research, 38124 Braunschweig, Germany; and.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Uckert</LastName><ForeName>Wolfgang</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Max-Delbrück-Center for Molecular Medicine, 13125 Berlin, Germany; Institute of Biology, Humboldt University Berlin, 10115 Berlin, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Schüler</LastName><ForeName>Thomas</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Institute of Molecular and Clinical Immunology, Medical Faculty, Otto-von-Guericke University, 39120 Magdeburg, Germany; Institute of Immunology, Charité Berlin, 12200 Berlin, Germany; thomas.schueler@med.ovgu.de.</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>2014</Year><Month>12</Month><Day>05</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Immunol</MedlineTA><NlmUniqueID>2985117R</NlmUniqueID><ISSNLinking>0022-1767</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C491198">Eomes protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D019253">Proto-Oncogene Proteins c-bcl-2</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011948">Receptors, Antigen, T-Cell</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017471">Receptors, Interferon</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D020825">T-Box Domain Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>07MXG07O12</RegistryNumber><NameOfSubstance UI="C078577">interferon gamma receptor</NameOfSubstance></Chemical><Chemical><RegistryNumber>114100-40-2</RegistryNumber><NameOfSubstance UI="C052617">Bcl2 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>126880-86-2</RegistryNumber><NameOfSubstance UI="D019041">L-Selectin</NameOfSubstance></Chemical><Chemical><RegistryNumber>82115-62-6</RegistryNumber><NameOfSubstance UI="D007371">Interferon-gamma</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.1.1</RegistryNumber><NameOfSubstance UI="D058570">TOR Serine-Threonine Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.1.1</RegistryNumber><NameOfSubstance UI="C546843">mTOR protein, mouse</NameOfSubstance></Chemical></ChemicalList><CitationSubset>AIM</CitationSubset><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018414" MajorTopicYN="N">CD8-Positive T-Lymphocytes</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002454" MajorTopicYN="N">Cell Differentiation</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002470" MajorTopicYN="N">Cell Survival</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007156" MajorTopicYN="N">Immunologic Memory</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007371" MajorTopicYN="N">Interferon-gamma</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019041" MajorTopicYN="N">L-Selectin</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018345" MajorTopicYN="N">Mice, Knockout</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019253" MajorTopicYN="N">Proto-Oncogene Proteins c-bcl-2</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011948" MajorTopicYN="N">Receptors, Antigen, T-Cell</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017471" MajorTopicYN="N">Receptors, Interferon</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020825" MajorTopicYN="N">T-Box Domain Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D058570" MajorTopicYN="N">TOR Serine-Threonine Kinases</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2014</Year><Month>12</Month><Day>7</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2014</Year><Month>12</Month><Day>7</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2015</Year><Month>3</Month><Day>12</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">25480562</ArticleId><ArticleId IdType="pii">jimmunol.1402058</ArticleId><ArticleId IdType="doi">10.4049/jimmunol.1402058</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Allemagne</li></country><region><li>Berlin</li></region><settlement><li>Berlin</li></settlement></list><tree><noCountry><name sortKey="Nishanth, Gopala" sort="Nishanth, Gopala" uniqKey="Nishanth G" first="Gopala" last="Nishanth">Gopala Nishanth</name><name sortKey="Schluter, Dirk" sort="Schluter, Dirk" uniqKey="Schluter D" first="Dirk" last="Schlüter">Dirk Schlüter</name></noCountry><country name="Allemagne"><region name="Berlin"><name sortKey="Stoycheva, Diana" sort="Stoycheva, Diana" uniqKey="Stoycheva D" first="Diana" last="Stoycheva">Diana Stoycheva</name></region><name sortKey="Deiser, Katrin" sort="Deiser, Katrin" uniqKey="Deiser K" first="Katrin" last="Deiser">Katrin Deiser</name><name sortKey="Schuler, Thomas" sort="Schuler, Thomas" uniqKey="Schuler T" first="Thomas" last="Schüler">Thomas Schüler</name><name sortKey="St Rck, Lilian" sort="St Rck, Lilian" uniqKey="St Rck L" first="Lilian" last="St Rck">Lilian St Rck</name><name sortKey="Uckert, Wolfgang" sort="Uckert, Wolfgang" uniqKey="Uckert W" first="Wolfgang" last="Uckert">Wolfgang Uckert</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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}}
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