Survival of effector CD8+ T cells during influenza infection is dependent on autophagy.
Identifieur interne : 000431 ( PubMed/Corpus ); précédent : 000430; suivant : 000432Survival of effector CD8+ T cells during influenza infection is dependent on autophagy.
Auteurs : Katrin Schlie ; Ashley Westerback ; Lindsay Devorkin ; Luke R. Hughson ; Jillian M. Brandon ; Sarah Macpherson ; Izabelle Gadawski ; Katelin N. Townsend ; Vincent I. Poon ; Mary A. Elrick ; Helene C F. Côté ; Ninan Abraham ; E John Wherry ; Noboru Mizushima ; Julian J. LumSource :
- Journal of immunology (Baltimore, Md. : 1950) [ 1550-6606 ] ; 2015.
English descriptors
- KwdEn :
- Animals, Autophagy (genetics), Autophagy (immunology), Autophagy-Related Protein 5, CD8-Positive T-Lymphocytes (immunology), CD8-Positive T-Lymphocytes (metabolism), Cell Survival (genetics), Cell Survival (immunology), Female, Gene Expression, Hypoxia (metabolism), Immunologic Memory, Influenza A virus (immunology), Mice, Mice, Knockout, Microtubule-Associated Proteins (genetics), Orthomyxoviridae Infections (immunology), Orthomyxoviridae Infections (metabolism), Reactive Oxygen Species (metabolism), T-Lymphocyte Subsets (immunology), T-Lymphocyte Subsets (metabolism), Tumor Suppressor Protein p53 (genetics), Tumor Suppressor Protein p53 (metabolism).
- MESH :
- chemical , genetics : Microtubule-Associated Proteins, Tumor Suppressor Protein p53.
- chemical , metabolism : Reactive Oxygen Species, Tumor Suppressor Protein p53.
- chemical : Autophagy-Related Protein 5.
- genetics : Autophagy, Cell Survival.
- immunology : Autophagy, CD8-Positive T-Lymphocytes, Cell Survival, Influenza A virus, Orthomyxoviridae Infections, T-Lymphocyte Subsets.
- metabolism : CD8-Positive T-Lymphocytes, Hypoxia, Orthomyxoviridae Infections, T-Lymphocyte Subsets.
- Animals, Female, Gene Expression, Immunologic Memory, Mice, Mice, Knockout.
Abstract
The activation and expansion of effector CD8(+) T cells are essential for controlling viral infections and tumor surveillance. During an immune response, T cells encounter extrinsic and intrinsic factors, including oxidative stress, nutrient availability, and inflammation, that can modulate their capacity to activate, proliferate, and survive. The dependency of T cells on autophagy for in vitro and in vivo activation, expansion, and memory remains unclear. Moreover, the specific signals and mechanisms that activate autophagy in T effector cells and their survival are not known. In this study, we generated a novel inducible autophagy knockout mouse to study T cell effector responses during the course of a virus infection. In response to influenza infection, Atg5(-/-) CD8(+) T cells had a decreased capacity to reach the peak effector response and were unable to maintain cell viability during the effector phase. As a consequence of Atg5 deletion and the impairment in effector-to-memory cell survival, mice fail to mount a memory response following a secondary challenge. We found that Atg5(-/-) effector CD8(+) T cells upregulated p53, a transcriptional state that was concomitant with widespread hypoxia in lymphoid tissues of infected mice. The onset of p53 activation was concurrent with higher levels of reactive oxygen species (ROS) that resulted in ROS-dependent apoptotic cell death, a fate that could be rescued by treating with the ROS scavenger N-acetylcysteine. Collectively, these results demonstrate that effector CD8(+) T cells require autophagy to suppress cell death and maintain survival in response to a viral infection.
DOI: 10.4049/jimmunol.1402571
PubMed: 25833396
Links to Exploration step
pubmed:25833396Le document en format XML
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Lum</name><affiliation><nlm:affiliation>Trev and Joyce Deeley Research Centre, British Columbia Cancer Agency, Victoria, British Columbia V8R 6V5, Canada; Department of Biochemistry and Microbiology, University of Victoria, Victoria, British Columbia V8W 3P6, Canada; jjlum@bccancer.bc.ca.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2015">2015</date><idno type="RBID">pubmed:25833396</idno><idno type="pmid">25833396</idno><idno type="doi">10.4049/jimmunol.1402571</idno><idno type="wicri:Area/PubMed/Corpus">000431</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000431</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Survival of effector CD8+ T cells during influenza infection is dependent on autophagy.</title><author><name sortKey="Schlie, Katrin" sort="Schlie, Katrin" uniqKey="Schlie K" first="Katrin" last="Schlie">Katrin Schlie</name><affiliation><nlm:affiliation>Trev and Joyce Deeley Research Centre, British Columbia Cancer Agency, Victoria, British Columbia V8R 6V5, Canada;</nlm:affiliation></affiliation></author><author><name sortKey="Westerback, Ashley" sort="Westerback, Ashley" uniqKey="Westerback A" first="Ashley" last="Westerback">Ashley Westerback</name><affiliation><nlm:affiliation>Trev and Joyce Deeley Research Centre, British Columbia Cancer Agency, Victoria, British Columbia V8R 6V5, Canada;</nlm:affiliation></affiliation></author><author><name sortKey="Devorkin, Lindsay" sort="Devorkin, Lindsay" uniqKey="Devorkin L" first="Lindsay" last="Devorkin">Lindsay Devorkin</name><affiliation><nlm:affiliation>Trev and Joyce Deeley Research Centre, British Columbia Cancer Agency, Victoria, British Columbia V8R 6V5, Canada; Department of Biochemistry and Microbiology, University of Victoria, Victoria, British Columbia V8W 3P6, Canada;</nlm:affiliation></affiliation></author><author><name sortKey="Hughson, Luke R" sort="Hughson, Luke R" uniqKey="Hughson L" first="Luke R" last="Hughson">Luke R. Hughson</name><affiliation><nlm:affiliation>Trev and Joyce Deeley Research Centre, British Columbia Cancer Agency, Victoria, British Columbia V8R 6V5, Canada; Department of Biochemistry and Microbiology, University of Victoria, Victoria, British Columbia V8W 3P6, Canada;</nlm:affiliation></affiliation></author><author><name sortKey="Brandon, Jillian M" sort="Brandon, Jillian M" uniqKey="Brandon J" first="Jillian M" last="Brandon">Jillian M. Brandon</name><affiliation><nlm:affiliation>Trev and Joyce Deeley Research Centre, British Columbia Cancer Agency, Victoria, British Columbia V8R 6V5, Canada;</nlm:affiliation></affiliation></author><author><name sortKey="Macpherson, Sarah" sort="Macpherson, Sarah" uniqKey="Macpherson S" first="Sarah" last="Macpherson">Sarah Macpherson</name><affiliation><nlm:affiliation>Trev and Joyce Deeley Research Centre, British Columbia Cancer Agency, Victoria, British Columbia V8R 6V5, Canada; Department of Biochemistry and Microbiology, University of Victoria, Victoria, British Columbia V8W 3P6, Canada;</nlm:affiliation></affiliation></author><author><name sortKey="Gadawski, Izabelle" sort="Gadawski, Izabelle" uniqKey="Gadawski I" first="Izabelle" last="Gadawski">Izabelle Gadawski</name><affiliation><nlm:affiliation>Department of Pathology and Laboratory Medicine, Centre for Blood Research, University of British Columbia, Vancouver, British Columbia V6T 1Z3, Canada;</nlm:affiliation></affiliation></author><author><name sortKey="Townsend, Katelin N" sort="Townsend, Katelin N" uniqKey="Townsend K" first="Katelin N" last="Townsend">Katelin N. Townsend</name><affiliation><nlm:affiliation>Trev and Joyce Deeley Research Centre, British Columbia Cancer Agency, Victoria, British Columbia V8R 6V5, Canada; Department of Biochemistry and Microbiology, University of Victoria, Victoria, British Columbia V8W 3P6, Canada;</nlm:affiliation></affiliation></author><author><name sortKey="Poon, Vincent I" sort="Poon, Vincent I" uniqKey="Poon V" first="Vincent I" last="Poon">Vincent I. Poon</name><affiliation><nlm:affiliation>Trev and Joyce Deeley Research Centre, British Columbia Cancer Agency, Victoria, British Columbia V8R 6V5, Canada; Department of Biochemistry and Microbiology, University of Victoria, Victoria, British Columbia V8W 3P6, Canada;</nlm:affiliation></affiliation></author><author><name sortKey="Elrick, Mary A" sort="Elrick, Mary A" uniqKey="Elrick M" first="Mary A" last="Elrick">Mary A. Elrick</name><affiliation><nlm:affiliation>Trev and Joyce Deeley Research Centre, British Columbia Cancer Agency, Victoria, British Columbia V8R 6V5, Canada; Department of Biochemistry and Microbiology, University of Victoria, Victoria, British Columbia V8W 3P6, Canada;</nlm:affiliation></affiliation></author><author><name sortKey="Cote, Helene C F" sort="Cote, Helene C F" uniqKey="Cote H" first="Helene C F" last="Côté">Helene C F. Côté</name><affiliation><nlm:affiliation>Department of Pathology and Laboratory Medicine, Centre for Blood Research, University of British Columbia, Vancouver, British Columbia V6T 1Z3, Canada;</nlm:affiliation></affiliation></author><author><name sortKey="Abraham, Ninan" sort="Abraham, Ninan" uniqKey="Abraham N" first="Ninan" last="Abraham">Ninan Abraham</name><affiliation><nlm:affiliation>Department of Zoology, Life Sciences Institute, University of British Columbia, Vancouver, British Columbia V6T 1Z3, Canada; Department of Microbiology and Immunology, Life Sciences Institute, University of British Columbia, Vancouver, British Columbia V6T 1Z3, Canada;</nlm:affiliation></affiliation></author><author><name sortKey="Wherry, E John" sort="Wherry, E John" uniqKey="Wherry E" first="E John" last="Wherry">E John Wherry</name><affiliation><nlm:affiliation>Department of Microbiology and Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104; and.</nlm:affiliation></affiliation></author><author><name sortKey="Mizushima, Noboru" sort="Mizushima, Noboru" uniqKey="Mizushima N" first="Noboru" last="Mizushima">Noboru Mizushima</name><affiliation><nlm:affiliation>Department of Biochemistry and Molecular Biology, Graduate School and Faculty of Medicine, University of Tokyo, Tokyo 113-0033, Japan.</nlm:affiliation></affiliation></author><author><name sortKey="Lum, Julian J" sort="Lum, Julian J" uniqKey="Lum J" first="Julian J" last="Lum">Julian J. Lum</name><affiliation><nlm:affiliation>Trev and Joyce Deeley Research Centre, British Columbia Cancer Agency, Victoria, British Columbia V8R 6V5, Canada; Department of Biochemistry and Microbiology, University of Victoria, Victoria, British Columbia V8W 3P6, Canada; jjlum@bccancer.bc.ca.</nlm:affiliation></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</term><term>Autophagy (genetics)</term><term>Autophagy (immunology)</term><term>Autophagy-Related Protein 5</term><term>CD8-Positive T-Lymphocytes (immunology)</term><term>CD8-Positive T-Lymphocytes (metabolism)</term><term>Cell Survival (genetics)</term><term>Cell Survival (immunology)</term><term>Female</term><term>Gene Expression</term><term>Hypoxia (metabolism)</term><term>Immunologic Memory</term><term>Influenza A virus (immunology)</term><term>Mice</term><term>Mice, Knockout</term><term>Microtubule-Associated Proteins (genetics)</term><term>Orthomyxoviridae Infections (immunology)</term><term>Orthomyxoviridae Infections (metabolism)</term><term>Reactive Oxygen Species (metabolism)</term><term>T-Lymphocyte Subsets (immunology)</term><term>T-Lymphocyte Subsets (metabolism)</term><term>Tumor Suppressor Protein p53 (genetics)</term><term>Tumor Suppressor Protein p53 (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Microtubule-Associated Proteins</term><term>Tumor Suppressor Protein p53</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Reactive Oxygen Species</term><term>Tumor Suppressor Protein p53</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Autophagy-Related Protein 5</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Autophagy</term><term>Cell Survival</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Autophagy</term><term>CD8-Positive T-Lymphocytes</term><term>Cell Survival</term><term>Influenza A virus</term><term>Orthomyxoviridae Infections</term><term>T-Lymphocyte Subsets</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>CD8-Positive T-Lymphocytes</term><term>Hypoxia</term><term>Orthomyxoviridae Infections</term><term>T-Lymphocyte Subsets</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Female</term><term>Gene Expression</term><term>Immunologic Memory</term><term>Mice</term><term>Mice, Knockout</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The activation and expansion of effector CD8(+) T cells are essential for controlling viral infections and tumor surveillance. During an immune response, T cells encounter extrinsic and intrinsic factors, including oxidative stress, nutrient availability, and inflammation, that can modulate their capacity to activate, proliferate, and survive. The dependency of T cells on autophagy for in vitro and in vivo activation, expansion, and memory remains unclear. Moreover, the specific signals and mechanisms that activate autophagy in T effector cells and their survival are not known. In this study, we generated a novel inducible autophagy knockout mouse to study T cell effector responses during the course of a virus infection. In response to influenza infection, Atg5(-/-) CD8(+) T cells had a decreased capacity to reach the peak effector response and were unable to maintain cell viability during the effector phase. As a consequence of Atg5 deletion and the impairment in effector-to-memory cell survival, mice fail to mount a memory response following a secondary challenge. We found that Atg5(-/-) effector CD8(+) T cells upregulated p53, a transcriptional state that was concomitant with widespread hypoxia in lymphoid tissues of infected mice. The onset of p53 activation was concurrent with higher levels of reactive oxygen species (ROS) that resulted in ROS-dependent apoptotic cell death, a fate that could be rescued by treating with the ROS scavenger N-acetylcysteine. Collectively, these results demonstrate that effector CD8(+) T cells require autophagy to suppress cell death and maintain survival in response to a viral infection. </div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25833396</PMID><DateCompleted><Year>2015</Year><Month>06</Month><Day>30</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>25</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1550-6606</ISSN><JournalIssue CitedMedium="Internet"><Volume>194</Volume><Issue>9</Issue><PubDate><Year>2015</Year><Month>May</Month><Day>01</Day></PubDate></JournalIssue><Title>Journal of immunology (Baltimore, Md. : 1950)</Title><ISOAbbreviation>J. Immunol.</ISOAbbreviation></Journal><ArticleTitle>Survival of effector CD8+ T cells during influenza infection is dependent on autophagy.</ArticleTitle><Pagination><MedlinePgn>4277-86</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.4049/jimmunol.1402571</ELocationID><Abstract><AbstractText>The activation and expansion of effector CD8(+) T cells are essential for controlling viral infections and tumor surveillance. During an immune response, T cells encounter extrinsic and intrinsic factors, including oxidative stress, nutrient availability, and inflammation, that can modulate their capacity to activate, proliferate, and survive. The dependency of T cells on autophagy for in vitro and in vivo activation, expansion, and memory remains unclear. Moreover, the specific signals and mechanisms that activate autophagy in T effector cells and their survival are not known. In this study, we generated a novel inducible autophagy knockout mouse to study T cell effector responses during the course of a virus infection. In response to influenza infection, Atg5(-/-) CD8(+) T cells had a decreased capacity to reach the peak effector response and were unable to maintain cell viability during the effector phase. As a consequence of Atg5 deletion and the impairment in effector-to-memory cell survival, mice fail to mount a memory response following a secondary challenge. We found that Atg5(-/-) effector CD8(+) T cells upregulated p53, a transcriptional state that was concomitant with widespread hypoxia in lymphoid tissues of infected mice. The onset of p53 activation was concurrent with higher levels of reactive oxygen species (ROS) that resulted in ROS-dependent apoptotic cell death, a fate that could be rescued by treating with the ROS scavenger N-acetylcysteine. Collectively, these results demonstrate that effector CD8(+) T cells require autophagy to suppress cell death and maintain survival in response to a viral infection. </AbstractText><CopyrightInformation>Copyright © 2015 by The American Association of Immunologists, Inc.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Schlie</LastName><ForeName>Katrin</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Trev and Joyce Deeley Research Centre, British Columbia Cancer Agency, Victoria, British Columbia V8R 6V5, Canada;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Westerback</LastName><ForeName>Ashley</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Trev and Joyce Deeley Research Centre, British Columbia Cancer Agency, Victoria, British Columbia V8R 6V5, Canada;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>DeVorkin</LastName><ForeName>Lindsay</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Trev and Joyce Deeley Research Centre, British Columbia Cancer Agency, Victoria, British Columbia V8R 6V5, Canada; Department of Biochemistry and Microbiology, University of Victoria, Victoria, British Columbia V8W 3P6, Canada;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hughson</LastName><ForeName>Luke R</ForeName><Initials>LR</Initials><AffiliationInfo><Affiliation>Trev and Joyce Deeley Research Centre, British Columbia Cancer Agency, Victoria, British Columbia V8R 6V5, Canada; Department of Biochemistry and Microbiology, University of Victoria, Victoria, British Columbia V8W 3P6, Canada;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Brandon</LastName><ForeName>Jillian M</ForeName><Initials>JM</Initials><AffiliationInfo><Affiliation>Trev and Joyce Deeley Research Centre, British Columbia Cancer Agency, Victoria, British Columbia V8R 6V5, Canada;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>MacPherson</LastName><ForeName>Sarah</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Trev and Joyce Deeley Research Centre, British Columbia Cancer Agency, Victoria, British Columbia V8R 6V5, Canada; Department of Biochemistry and Microbiology, University of Victoria, Victoria, British Columbia V8W 3P6, Canada;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gadawski</LastName><ForeName>Izabelle</ForeName><Initials>I</Initials><AffiliationInfo><Affiliation>Department of Pathology and Laboratory Medicine, Centre for Blood Research, University of British Columbia, Vancouver, British Columbia V6T 1Z3, Canada;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Townsend</LastName><ForeName>Katelin N</ForeName><Initials>KN</Initials><AffiliationInfo><Affiliation>Trev and Joyce Deeley Research Centre, British Columbia Cancer Agency, Victoria, British Columbia V8R 6V5, Canada; Department of Biochemistry and Microbiology, University of Victoria, Victoria, British Columbia V8W 3P6, Canada;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Poon</LastName><ForeName>Vincent I</ForeName><Initials>VI</Initials><AffiliationInfo><Affiliation>Trev and Joyce Deeley Research Centre, British Columbia Cancer Agency, Victoria, British Columbia V8R 6V5, Canada; Department of Biochemistry and Microbiology, University of Victoria, Victoria, British Columbia V8W 3P6, Canada;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Elrick</LastName><ForeName>Mary A</ForeName><Initials>MA</Initials><AffiliationInfo><Affiliation>Trev and Joyce Deeley Research Centre, British Columbia Cancer Agency, Victoria, British Columbia V8R 6V5, Canada; Department of Biochemistry and Microbiology, University of Victoria, Victoria, British Columbia V8W 3P6, Canada;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Côté</LastName><ForeName>Helene C F</ForeName><Initials>HC</Initials><AffiliationInfo><Affiliation>Department of Pathology and Laboratory Medicine, Centre for Blood Research, University of British Columbia, Vancouver, British Columbia V6T 1Z3, Canada;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Abraham</LastName><ForeName>Ninan</ForeName><Initials>N</Initials><Identifier Source="ORCID">http://orcid.org/0000-0002-2747-1246</Identifier><AffiliationInfo><Affiliation>Department of Zoology, Life Sciences Institute, University of British Columbia, Vancouver, British Columbia V6T 1Z3, Canada; Department of Microbiology and Immunology, Life Sciences Institute, University of British Columbia, Vancouver, British Columbia V6T 1Z3, Canada;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wherry</LastName><ForeName>E John</ForeName><Initials>EJ</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104; and.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mizushima</LastName><ForeName>Noboru</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Department of Biochemistry and Molecular Biology, Graduate School and Faculty of Medicine, University of Tokyo, Tokyo 113-0033, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lum</LastName><ForeName>Julian J</ForeName><Initials>JJ</Initials><AffiliationInfo><Affiliation>Trev and Joyce Deeley Research Centre, British Columbia Cancer Agency, Victoria, British Columbia V8R 6V5, Canada; Department of Biochemistry and Microbiology, University of Victoria, Victoria, British Columbia V8W 3P6, Canada; jjlum@bccancer.bc.ca.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><DataBankList CompleteYN="Y"><DataBank><DataBankName>GEO</DataBankName><AccessionNumberList><AccessionNumber>GSE49254</AccessionNumber></AccessionNumberList></DataBank></DataBankList><GrantList CompleteYN="Y"><Grant><GrantID>MOP97909</GrantID><Agency>Canadian Institutes of Health Research</Agency><Country>Canada</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2015</Year><Month>04</Month><Day>01</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="C495773">Atg5 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance 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5</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018414" MajorTopicYN="N">CD8-Positive T-Lymphocytes</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</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="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015870" MajorTopicYN="N">Gene Expression</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000860" MajorTopicYN="N">Hypoxia</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007156" MajorTopicYN="N">Immunologic Memory</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009980" MajorTopicYN="N">Influenza A virus</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">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="D008869" MajorTopicYN="N">Microtubule-Associated Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009976" MajorTopicYN="N">Orthomyxoviridae Infections</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017382" MajorTopicYN="N">Reactive Oxygen Species</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016176" MajorTopicYN="N">T-Lymphocyte Subsets</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016159" MajorTopicYN="N">Tumor Suppressor Protein p53</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2014</Year><Month>10</Month><Day>09</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2015</Year><Month>02</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2015</Year><Month>4</Month><Day>3</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2015</Year><Month>4</Month><Day>3</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2015</Year><Month>7</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">25833396</ArticleId><ArticleId IdType="pii">jimmunol.1402571</ArticleId><ArticleId IdType="doi">10.4049/jimmunol.1402571</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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