Environmental cues regulate epigenetic reprogramming of airway-resident memory CD8+ T cells.
Identifieur interne : 000158 ( PubMed/Curation ); précédent : 000157; suivant : 000159Environmental cues regulate epigenetic reprogramming of airway-resident memory CD8+ T cells.
Auteurs : Sarah L. Hayward [États-Unis] ; Christopher D. Scharer [États-Unis] ; Emily K. Cartwright [États-Unis] ; Shiki Takamura [Japon] ; Zheng-Rong Tiger Li [États-Unis] ; Jeremy M. Boss [États-Unis] ; Jacob E. Kohlmeier [États-Unis]Source :
- Nature immunology [ 1529-2916 ] ; 2020.
Descripteurs français
- KwdFr :
- Animaux, Apoptose (immunologie), Femelle, Infections à Orthomyxoviridae (anatomopathologie), Infections à Orthomyxoviridae (génétique), Infections à Orthomyxoviridae (immunologie), Lymphocytes T CD8+ (cytologie), Lymphocytes T CD8+ (immunologie), Microenvironnement cellulaire (génétique), Microenvironnement cellulaire (immunologie), Mâle, Mémoire immunologique (génétique), Poumon (cytologie), Poumon (immunologie), Reprogrammation cellulaire (génétique), Reprogrammation cellulaire (immunologie), Souris, Souris de lignée C57BL, Survie cellulaire (génétique), Survie cellulaire (immunologie), Épigenèse génétique (immunologie).
- MESH :
- anatomopathologie : Infections à Orthomyxoviridae.
- cytologie : Lymphocytes T CD8+, Poumon.
- génétique : Infections à Orthomyxoviridae, Microenvironnement cellulaire, Mémoire immunologique, Reprogrammation cellulaire, Survie cellulaire.
- immunologie : Apoptose, Infections à Orthomyxoviridae, Lymphocytes T CD8+, Microenvironnement cellulaire, Poumon, Reprogrammation cellulaire, Survie cellulaire, Épigenèse génétique.
- Animaux, Femelle, Mâle, Souris, Souris de lignée C57BL.
English descriptors
- KwdEn :
- Animals, Apoptosis (immunology), CD8-Positive T-Lymphocytes (cytology), CD8-Positive T-Lymphocytes (immunology), Cell Survival (genetics), Cell Survival (immunology), Cellular Microenvironment (genetics), Cellular Microenvironment (immunology), Cellular Reprogramming (genetics), Cellular Reprogramming (immunology), Epigenesis, Genetic (immunology), Female, Immunologic Memory (genetics), Lung (cytology), Lung (immunology), Male, Mice, Mice, Inbred C57BL, Orthomyxoviridae Infections (genetics), Orthomyxoviridae Infections (immunology), Orthomyxoviridae Infections (pathology).
- MESH :
- cytology : CD8-Positive T-Lymphocytes, Lung.
- genetics : Cell Survival, Cellular Microenvironment, Cellular Reprogramming, Immunologic Memory, Orthomyxoviridae Infections.
- immunology : Apoptosis, CD8-Positive T-Lymphocytes, Cell Survival, Cellular Microenvironment, Cellular Reprogramming, Epigenesis, Genetic, Lung, Orthomyxoviridae Infections.
- pathology : Orthomyxoviridae Infections.
- Animals, Female, Male, Mice, Mice, Inbred C57BL.
Abstract
Tissue-resident memory T cells (TRM cells) are critical for cellular immunity to respiratory pathogens and reside in both the airways and the interstitium. In the present study, we found that the airway environment drove transcriptional and epigenetic changes that specifically regulated the cytolytic functions of airway TRM cells and promoted apoptosis due to amino acid starvation and activation of the integrated stress response. Comparison of airway TRM cells and splenic effector-memory T cells transferred into the airways indicated that the environment was necessary to activate these pathways, but did not induce TRM cell lineage reprogramming. Importantly, activation of the integrated stress response was reversed in airway TRM cells placed in a nutrient-rich environment. Our data defined the genetic programs of distinct lung TRM cell populations and show that local environmental cues altered airway TRM cells to limit cytolytic function and promote cell death, which ultimately leads to fewer TRM cells in the lung.
DOI: 10.1038/s41590-019-0584-x
PubMed: 31953534
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In the present study, we found that the airway environment drove transcriptional and epigenetic changes that specifically regulated the cytolytic functions of airway T<sub>RM</sub> cells and promoted apoptosis due to amino acid starvation and activation of the integrated stress response. Comparison of airway T<sub>RM</sub> cells and splenic effector-memory T cells transferred into the airways indicated that the environment was necessary to activate these pathways, but did not induce T<sub>RM</sub> cell lineage reprogramming. Importantly, activation of the integrated stress response was reversed in airway T<sub>RM</sub> cells placed in a nutrient-rich environment. Our data defined the genetic programs of distinct lung T<sub>RM</sub> cell populations and show that local environmental cues altered airway T<sub>RM</sub> cells to limit cytolytic function and promote cell death, which ultimately leads to fewer T<sub>RM</sub> cells in the lung.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">31953534</PMID><DateCompleted><Year>2020</Year><Month>04</Month><Day>20</Day></DateCompleted><DateRevised><Year>2020</Year><Month>04</Month><Day>20</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1529-2916</ISSN><JournalIssue CitedMedium="Internet"><Volume>21</Volume><Issue>3</Issue><PubDate><Year>2020</Year><Month>03</Month></PubDate></JournalIssue><Title>Nature immunology</Title><ISOAbbreviation>Nat. Immunol.</ISOAbbreviation></Journal><ArticleTitle>Environmental cues regulate epigenetic reprogramming of airway-resident memory CD8<sup>+</sup> T cells.</ArticleTitle><Pagination><MedlinePgn>309-320</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1038/s41590-019-0584-x</ELocationID><Abstract><AbstractText>Tissue-resident memory T cells (T<sub>RM</sub> cells) are critical for cellular immunity to respiratory pathogens and reside in both the airways and the interstitium. In the present study, we found that the airway environment drove transcriptional and epigenetic changes that specifically regulated the cytolytic functions of airway T<sub>RM</sub> cells and promoted apoptosis due to amino acid starvation and activation of the integrated stress response. Comparison of airway T<sub>RM</sub> cells and splenic effector-memory T cells transferred into the airways indicated that the environment was necessary to activate these pathways, but did not induce T<sub>RM</sub> cell lineage reprogramming. Importantly, activation of the integrated stress response was reversed in airway T<sub>RM</sub> cells placed in a nutrient-rich environment. Our data defined the genetic programs of distinct lung T<sub>RM</sub> cell populations and show that local environmental cues altered airway T<sub>RM</sub> cells to limit cytolytic function and promote cell death, which ultimately leads to fewer T<sub>RM</sub> cells in the lung.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Hayward</LastName><ForeName>Sarah L</ForeName><Initials>SL</Initials><Identifier Source="ORCID">0000-0001-7052-5556</Identifier><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, GA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Scharer</LastName><ForeName>Christopher D</ForeName><Initials>CD</Initials><Identifier Source="ORCID">0000-0001-7716-8504</Identifier><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, GA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cartwright</LastName><ForeName>Emily K</ForeName><Initials>EK</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, GA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Takamura</LastName><ForeName>Shiki</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Immunology, Kindai University Faculty of Medicine, Osaka-Sayama, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Zheng-Rong Tiger</ForeName><Initials>ZT</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, GA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Boss</LastName><ForeName>Jeremy M</ForeName><Initials>JM</Initials><Identifier Source="ORCID">0000-0002-2432-1840</Identifier><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, GA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kohlmeier</LastName><ForeName>Jacob E</ForeName><Initials>JE</Initials><Identifier Source="ORCID">0000-0002-7209-6641</Identifier><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, GA, USA. jkohlmeier@emory.edu.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Emory-UGA Center of Excellence for Influenza Research and Surveillance, Atlanta, GA, USA. jkohlmeier@emory.edu.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>HHSN272201300006C</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HL122559</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P01 AI125180</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>F31 HL136101</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>HHSN272201400004C</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 AI113021</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HL138508</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>01</Month><Day>17</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Nat Immunol</MedlineTA><NlmUniqueID>100941354</NlmUniqueID><ISSNLinking>1529-2908</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018414" MajorTopicYN="N">CD8-Positive T-Lymphocytes</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</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="D060833" MajorTopicYN="N">Cellular Microenvironment</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D065150" MajorTopicYN="N">Cellular Reprogramming</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D044127" MajorTopicYN="N">Epigenesis, Genetic</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007156" MajorTopicYN="N">Immunologic Memory</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008168" 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