Plasmacytoid dendritic cells enhance mortality during lethal influenza infections by eliminating virus-specific CD8 T cells.
Identifieur interne : 000207 ( PubMed/Corpus ); précédent : 000206; suivant : 000208Plasmacytoid dendritic cells enhance mortality during lethal influenza infections by eliminating virus-specific CD8 T cells.
Auteurs : Ryan A. Langlois ; Kevin L. LeggeSource :
- Journal of immunology (Baltimore, Md. : 1950) [ 1550-6606 ] ; 2010.
English descriptors
- KwdEn :
- Adoptive Transfer, Animals, Apoptosis (immunology), CD8 Antigens (biosynthesis), CD8-Positive T-Lymphocytes (immunology), CD8-Positive T-Lymphocytes (metabolism), CD8-Positive T-Lymphocytes (pathology), Cell Movement (immunology), Dendritic Cells (immunology), Dendritic Cells (metabolism), Dendritic Cells (transplantation), Down-Regulation (immunology), Fas Ligand Protein (antagonists & inhibitors), Fas Ligand Protein (biosynthesis), Fas Ligand Protein (physiology), Immunophenotyping, Influenza A Virus, H1N1 Subtype (immunology), Influenza A Virus, H2N2 Subtype (immunology), Lymph Nodes (immunology), Lymph Nodes (pathology), Lymph Nodes (virology), Lymphocyte Activation (immunology), Lymphocyte Count, Lymphocyte Depletion (methods), Mice, Mice, Inbred BALB C, Mice, Transgenic, Orthomyxoviridae Infections (immunology), Orthomyxoviridae Infections (mortality), Orthomyxoviridae Infections (pathology), fas Receptor (biosynthesis), fas Receptor (physiology).
- MESH :
- chemical , antagonists & inhibitors : Fas Ligand Protein.
- chemical , biosynthesis : CD8 Antigens, Fas Ligand Protein, fas Receptor.
- immunology : Apoptosis, CD8-Positive T-Lymphocytes, Cell Movement, Dendritic Cells, Down-Regulation, Influenza A Virus, H1N1 Subtype, Influenza A Virus, H2N2 Subtype, Lymph Nodes, Lymphocyte Activation, Orthomyxoviridae Infections.
- metabolism : CD8-Positive T-Lymphocytes, Dendritic Cells.
- methods : Lymphocyte Depletion.
- mortality : Orthomyxoviridae Infections.
- pathology : CD8-Positive T-Lymphocytes, Lymph Nodes, Orthomyxoviridae Infections.
- chemical , physiology : Fas Ligand Protein, fas Receptor.
- transplantation : Dendritic Cells.
- virology : Lymph Nodes.
- Adoptive Transfer, Animals, Immunophenotyping, Lymphocyte Count, Mice, Mice, Inbred BALB C, Mice, Transgenic.
Abstract
Previous studies have shown that the reduction in CD8 T cell immunity observed during high-dose influenza A virus (IAV) infection is mediated via lymph node (LN) dendritic cells (DCs) that express Fas ligand (FasL) and drive FasL-Fas (DC-T)-induced apoptosis. However, the specific DC subset(s) within the LN and the additional factors required for DC-mediated elimination of IAV-specific CD8 T cells remain unknown. In this paper, we demonstrate that plasmacytoid DCs (pDCs), which downregulate FasL during sublethal, but not lethal, IAV infection, accumulate to greater numbers within the LNs of lethal dose-infected mice. Further our findings show that pDCs from lethal, but not sublethal, dose IAV infections drive elimination of Fas(+) CD8 T cells and that this elimination occurs only in the absence of TCR recognition of IAV peptide-MHC class I complexes. Together, these results suggest that pDCs play a heretofore unknown deleterious role during lethal dose IAV infections by limiting the CD8 T cell response.
DOI: 10.4049/jimmunol.0902984
PubMed: 20220091
Links to Exploration step
pubmed:20220091Le document en format XML
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Legge</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2010">2010</date><idno type="RBID">pubmed:20220091</idno><idno type="pmid">20220091</idno><idno type="doi">10.4049/jimmunol.0902984</idno><idno type="wicri:Area/PubMed/Corpus">000207</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000207</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Plasmacytoid dendritic cells enhance mortality during lethal influenza infections by eliminating virus-specific CD8 T cells.</title><author><name sortKey="Langlois, Ryan A" sort="Langlois, Ryan A" uniqKey="Langlois R" first="Ryan A" last="Langlois">Ryan A. Langlois</name><affiliation><nlm:affiliation>Department of Pathology, University of Iowa, Iowa City, IA 52242, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Legge, Kevin L" sort="Legge, Kevin L" uniqKey="Legge K" first="Kevin L" last="Legge">Kevin L. 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However, the specific DC subset(s) within the LN and the additional factors required for DC-mediated elimination of IAV-specific CD8 T cells remain unknown. In this paper, we demonstrate that plasmacytoid DCs (pDCs), which downregulate FasL during sublethal, but not lethal, IAV infection, accumulate to greater numbers within the LNs of lethal dose-infected mice. Further our findings show that pDCs from lethal, but not sublethal, dose IAV infections drive elimination of Fas(+) CD8 T cells and that this elimination occurs only in the absence of TCR recognition of IAV peptide-MHC class I complexes. Together, these results suggest that pDCs play a heretofore unknown deleterious role during lethal dose IAV infections by limiting the CD8 T cell response.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">20220091</PMID><DateCompleted><Year>2010</Year><Month>05</Month><Day>27</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1550-6606</ISSN><JournalIssue CitedMedium="Internet"><Volume>184</Volume><Issue>8</Issue><PubDate><Year>2010</Year><Month>Apr</Month><Day>15</Day></PubDate></JournalIssue><Title>Journal of immunology (Baltimore, Md. : 1950)</Title><ISOAbbreviation>J. Immunol.</ISOAbbreviation></Journal><ArticleTitle>Plasmacytoid dendritic cells enhance mortality during lethal influenza infections by eliminating virus-specific CD8 T cells.</ArticleTitle><Pagination><MedlinePgn>4440-6</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.4049/jimmunol.0902984</ELocationID><Abstract><AbstractText>Previous studies have shown that the reduction in CD8 T cell immunity observed during high-dose influenza A virus (IAV) infection is mediated via lymph node (LN) dendritic cells (DCs) that express Fas ligand (FasL) and drive FasL-Fas (DC-T)-induced apoptosis. However, the specific DC subset(s) within the LN and the additional factors required for DC-mediated elimination of IAV-specific CD8 T cells remain unknown. In this paper, we demonstrate that plasmacytoid DCs (pDCs), which downregulate FasL during sublethal, but not lethal, IAV infection, accumulate to greater numbers within the LNs of lethal dose-infected mice. Further our findings show that pDCs from lethal, but not sublethal, dose IAV infections drive elimination of Fas(+) CD8 T cells and that this elimination occurs only in the absence of TCR recognition of IAV peptide-MHC class I complexes. Together, these results suggest that pDCs play a heretofore unknown deleterious role during lethal dose IAV infections by limiting the CD8 T cell response.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Langlois</LastName><ForeName>Ryan A</ForeName><Initials>RA</Initials><AffiliationInfo><Affiliation>Department of Pathology, University of Iowa, Iowa City, IA 52242, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Legge</LastName><ForeName>Kevin L</ForeName><Initials>KL</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>AI-076989</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 AI071085</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R21 AI076989-01</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>AI-071085</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 AI071085-03</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 AI071085-02</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R21 AI076989-02</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R56 AI071085</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R21 AI076989</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 AI071085-01A1</GrantID><Acronym>AI</Acronym><Agency>NIAID 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><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2010</Year><Month>03</Month><Day>10</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="D016827">CD8 Antigens</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C431698">CD8alpha antigen</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D053222">Fas Ligand Protein</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C505658">Fasl protein, 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