Differential response of respiratory dendritic cell subsets to influenza virus infection.
Identifieur interne : 000264 ( PubMed/Corpus ); précédent : 000263; suivant : 000265Differential response of respiratory dendritic cell subsets to influenza virus infection.
Auteurs : Xueli Hao ; Taeg S. Kim ; Thomas J. BracialeSource :
- Journal of virology [ 1098-5514 ] ; 2008.
English descriptors
- KwdEn :
- Animals, Antigens, CD (analysis), CD11b Antigen (analysis), CD11c Antigen (analysis), Cytokines (biosynthesis), Dendritic Cells (chemistry), Dendritic Cells (immunology), Female, Flow Cytometry, Influenza A Virus, H2N2 Subtype (immunology), Integrin alpha Chains (analysis), Leukocyte Common Antigens (analysis), Mice, Mice, Inbred BALB C, Orthomyxoviridae Infections (immunology), Respiratory System (immunology), Respiratory System (virology).
- MESH :
- chemical , analysis : Antigens, CD, CD11b Antigen, CD11c Antigen, Integrin alpha Chains, Leukocyte Common Antigens.
- chemical , biosynthesis : Cytokines.
- chemistry : Dendritic Cells.
- immunology : Dendritic Cells, Influenza A Virus, H2N2 Subtype, Orthomyxoviridae Infections, Respiratory System.
- virology : Respiratory System.
- Animals, Female, Flow Cytometry, Mice, Mice, Inbred BALB C.
Abstract
Dendritic cells (DC) are believed to play an important role in the initiation of innate and adaptive immune responses to infection, including respiratory tract infections, where respiratory DC (RDC) perform this role. In this report, we examined the susceptibilities of isolated murine RDC to influenza virus infection in vitro and the effect of the multiplicity of infection (MOI) on costimulatory ligand upregulation and inflammatory cytokine/chemokine production after infection. We found that the efficiency of influenza virus infection of RDC increased with increasing MOIs. Furthermore, distinct subpopulations of RDC differed in their susceptibilities to influenza virus infection and in the magnitude/tempo of costimulatory ligand expression. Additional characterization of the CD11c-positive (CD11c(+)) RDC revealed that the identifiable subsets of RDC differed in susceptibility to infection, with CD11c(+) CD103(+) DC exhibiting the greatest susceptibility, CD11c(+) CD11b(hi) DC exhibiting intermediate susceptibility, and CD11c(+) B220(+) plasmacytoid DC (pDC) exhibiting the least susceptibility to infection. A companion analysis of the in vivo susceptibilities of these RDC subsets to influenza virus revealed a corresponding infection pattern. The three RDC subsets displayed different patterns of cytokine/chemokine production in response to influenza virus infection in vitro: pDC were the predominant producers of most cytokines examined, while CD103(+) DC and CD11b(hi) DC produced elevated levels of the murine chemokine CXCL1 (KC), interleukin 12p40, and RANTES in response to influenza virus infection. Our results indicate that RDC are targets of influenza virus infection and that distinct RDC subsets differ in their susceptibilities and responses to infection.
DOI: 10.1128/JVI.02367-07
PubMed: 18353940
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pubmed:18353940Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Differential response of respiratory dendritic cell subsets to influenza virus infection.</title><author><name sortKey="Hao, Xueli" sort="Hao, Xueli" uniqKey="Hao X" first="Xueli" last="Hao">Xueli Hao</name><affiliation><nlm:affiliation>Carter Immunology Center, UVA, P.O. Box 801386, Charlottesville, VA 22908, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Kim, Taeg S" sort="Kim, Taeg S" uniqKey="Kim T" first="Taeg S" last="Kim">Taeg S. Kim</name></author><author><name sortKey="Braciale, Thomas J" sort="Braciale, Thomas J" uniqKey="Braciale T" first="Thomas J" last="Braciale">Thomas J. Braciale</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2008">2008</date><idno type="RBID">pubmed:18353940</idno><idno type="pmid">18353940</idno><idno type="doi">10.1128/JVI.02367-07</idno><idno type="wicri:Area/PubMed/Corpus">000264</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000264</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Differential response of respiratory dendritic cell subsets to influenza virus infection.</title><author><name sortKey="Hao, Xueli" sort="Hao, Xueli" uniqKey="Hao X" first="Xueli" last="Hao">Xueli Hao</name><affiliation><nlm:affiliation>Carter Immunology Center, UVA, P.O. Box 801386, Charlottesville, VA 22908, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Kim, Taeg S" sort="Kim, Taeg S" uniqKey="Kim T" first="Taeg S" last="Kim">Taeg S. Kim</name></author><author><name sortKey="Braciale, Thomas J" sort="Braciale, Thomas J" uniqKey="Braciale T" first="Thomas J" last="Braciale">Thomas J. Braciale</name></author></analytic><series><title level="j">Journal of virology</title><idno type="eISSN">1098-5514</idno><imprint><date when="2008" type="published">2008</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Antigens, CD (analysis)</term><term>CD11b Antigen (analysis)</term><term>CD11c Antigen (analysis)</term><term>Cytokines (biosynthesis)</term><term>Dendritic Cells (chemistry)</term><term>Dendritic Cells (immunology)</term><term>Female</term><term>Flow Cytometry</term><term>Influenza A Virus, H2N2 Subtype (immunology)</term><term>Integrin alpha Chains (analysis)</term><term>Leukocyte Common Antigens (analysis)</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>Orthomyxoviridae Infections (immunology)</term><term>Respiratory System (immunology)</term><term>Respiratory System (virology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>Antigens, CD</term><term>CD11b Antigen</term><term>CD11c Antigen</term><term>Integrin alpha Chains</term><term>Leukocyte Common Antigens</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Cytokines</term></keywords><keywords scheme="MESH" qualifier="chemistry" xml:lang="en"><term>Dendritic Cells</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Dendritic Cells</term><term>Influenza A Virus, H2N2 Subtype</term><term>Orthomyxoviridae Infections</term><term>Respiratory System</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Respiratory System</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Female</term><term>Flow Cytometry</term><term>Mice</term><term>Mice, Inbred BALB C</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Dendritic cells (DC) are believed to play an important role in the initiation of innate and adaptive immune responses to infection, including respiratory tract infections, where respiratory DC (RDC) perform this role. In this report, we examined the susceptibilities of isolated murine RDC to influenza virus infection in vitro and the effect of the multiplicity of infection (MOI) on costimulatory ligand upregulation and inflammatory cytokine/chemokine production after infection. We found that the efficiency of influenza virus infection of RDC increased with increasing MOIs. Furthermore, distinct subpopulations of RDC differed in their susceptibilities to influenza virus infection and in the magnitude/tempo of costimulatory ligand expression. Additional characterization of the CD11c-positive (CD11c(+)) RDC revealed that the identifiable subsets of RDC differed in susceptibility to infection, with CD11c(+) CD103(+) DC exhibiting the greatest susceptibility, CD11c(+) CD11b(hi) DC exhibiting intermediate susceptibility, and CD11c(+) B220(+) plasmacytoid DC (pDC) exhibiting the least susceptibility to infection. A companion analysis of the in vivo susceptibilities of these RDC subsets to influenza virus revealed a corresponding infection pattern. The three RDC subsets displayed different patterns of cytokine/chemokine production in response to influenza virus infection in vitro: pDC were the predominant producers of most cytokines examined, while CD103(+) DC and CD11b(hi) DC produced elevated levels of the murine chemokine CXCL1 (KC), interleukin 12p40, and RANTES in response to influenza virus infection. Our results indicate that RDC are targets of influenza virus infection and that distinct RDC subsets differ in their susceptibilities and responses to infection.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">18353940</PMID><DateCompleted><Year>2008</Year><Month>05</Month><Day>13</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1098-5514</ISSN><JournalIssue CitedMedium="Internet"><Volume>82</Volume><Issue>10</Issue><PubDate><Year>2008</Year><Month>May</Month></PubDate></JournalIssue><Title>Journal of virology</Title><ISOAbbreviation>J. Virol.</ISOAbbreviation></Journal><ArticleTitle>Differential response of respiratory dendritic cell subsets to influenza virus infection.</ArticleTitle><Pagination><MedlinePgn>4908-19</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1128/JVI.02367-07</ELocationID><Abstract><AbstractText>Dendritic cells (DC) are believed to play an important role in the initiation of innate and adaptive immune responses to infection, including respiratory tract infections, where respiratory DC (RDC) perform this role. In this report, we examined the susceptibilities of isolated murine RDC to influenza virus infection in vitro and the effect of the multiplicity of infection (MOI) on costimulatory ligand upregulation and inflammatory cytokine/chemokine production after infection. We found that the efficiency of influenza virus infection of RDC increased with increasing MOIs. Furthermore, distinct subpopulations of RDC differed in their susceptibilities to influenza virus infection and in the magnitude/tempo of costimulatory ligand expression. Additional characterization of the CD11c-positive (CD11c(+)) RDC revealed that the identifiable subsets of RDC differed in susceptibility to infection, with CD11c(+) CD103(+) DC exhibiting the greatest susceptibility, CD11c(+) CD11b(hi) DC exhibiting intermediate susceptibility, and CD11c(+) B220(+) plasmacytoid DC (pDC) exhibiting the least susceptibility to infection. A companion analysis of the in vivo susceptibilities of these RDC subsets to influenza virus revealed a corresponding infection pattern. The three RDC subsets displayed different patterns of cytokine/chemokine production in response to influenza virus infection in vitro: pDC were the predominant producers of most cytokines examined, while CD103(+) DC and CD11b(hi) DC produced elevated levels of the murine chemokine CXCL1 (KC), interleukin 12p40, and RANTES in response to influenza virus infection. Our results indicate that RDC are targets of influenza virus infection and that distinct RDC subsets differ in their susceptibilities and responses to infection.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Hao</LastName><ForeName>Xueli</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Carter Immunology Center, UVA, P.O. Box 801386, Charlottesville, VA 22908, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Taeg S</ForeName><Initials>TS</Initials></Author><Author ValidYN="Y"><LastName>Braciale</LastName><ForeName>Thomas J</ForeName><Initials>TJ</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>AI-37293</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 AI037293</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>AI-15608</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R37 AI015608</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>HL-33391</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HL033391</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 AI015608</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>AI-57168</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>U54 AI057168</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HL033391-27</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 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