Inflammation conditions mature dendritic cells to retain the capacity to present new antigens but with altered cytokine secretion function.
Identifieur interne : 003320 ( PubMed/Curation ); précédent : 003319; suivant : 003321Inflammation conditions mature dendritic cells to retain the capacity to present new antigens but with altered cytokine secretion function.
Auteurs : Javier Vega-Ramos [Australie] ; Antoine Roquilly [Australie] ; Yifan Zhan [Australie] ; Louise J. Young [Australie] ; Justine D. Mintern [Australie] ; Jose A. Villadangos [Australie]Source :
- Journal of immunology (Baltimore, Md. : 1950) [ 1550-6606 ] ; 2014.
Descripteurs français
- KwdFr :
- Activation des lymphocytes (immunologie), Animaux, Antigènes CD8 (biosynthèse), Antigènes d'histocompatibilité de classe II (biosynthèse), Cellules dendritiques (immunologie), Cytokines (immunologie), Différenciation cellulaire (immunologie), Facteur de nécrose tumorale alpha (biosynthèse), Inflammation (immunologie), Lymphocytes T (immunologie), Médiateurs de l'inflammation (immunologie), Ovalbumine (immunologie), Présentation d'antigène (immunologie), Récepteur-9 de type Toll-like (génétique), Récepteur-9 de type Toll-like (immunologie), Souris, Souris de lignée C57BL, Souris de lignée CBA, Souris knockout, Ubiquitin-protein ligases (biosynthèse).
- MESH :
- biosynthèse : Antigènes CD8, Antigènes d'histocompatibilité de classe II, Facteur de nécrose tumorale alpha, Ubiquitin-protein ligases.
- génétique : Récepteur-9 de type Toll-like.
- immunologie : Activation des lymphocytes, Cellules dendritiques, Cytokines, Différenciation cellulaire, Inflammation, Lymphocytes T, Médiateurs de l'inflammation, Ovalbumine, Présentation d'antigène, Récepteur-9 de type Toll-like.
- Animaux, Souris, Souris de lignée C57BL, Souris de lignée CBA, Souris knockout.
English descriptors
- KwdEn :
- Animals, Antigen Presentation (immunology), Antigens, CD8 (biosynthesis), Cell Differentiation (immunology), Cytokines (immunology), Dendritic Cells (immunology), Histocompatibility Antigens Class II (biosynthesis), Inflammation (immunology), Inflammation Mediators (immunology), Lymphocyte Activation (immunology), Mice, Mice, Inbred C57BL, Mice, Inbred CBA, Mice, Knockout, Ovalbumin (immunology), T-Lymphocytes (immunology), Toll-Like Receptor 9 (genetics), Toll-Like Receptor 9 (immunology), Tumor Necrosis Factor-alpha (biosynthesis), Ubiquitin-Protein Ligases (biosynthesis).
- MESH :
- chemical , biosynthesis : Antigens, CD8, Histocompatibility Antigens Class II, Tumor Necrosis Factor-alpha, Ubiquitin-Protein Ligases.
- chemical , genetics : Toll-Like Receptor 9.
- immunology : Antigen Presentation, Cell Differentiation, Cytokines, Dendritic Cells, Inflammation, Inflammation Mediators, Lymphocyte Activation, Ovalbumin, T-Lymphocytes, Toll-Like Receptor 9.
- Animals, Mice, Mice, Inbred C57BL, Mice, Inbred CBA, Mice, Knockout.
Abstract
Dendritic cells (DCs) are directly activated by pathogen-associated molecular patterns (PAMPs) and undergo maturation. Mature DCs express high levels of MHC class II molecules ("signal 1"), upregulate T cell costimulatory receptors ("signal 2"), and secrete "signal 3" cytokines (e.g., IL-12). Mature DCs efficiently present Ags linked to the activating PAMP and prime naive T cells. However, mature DCs downregulate MHC II synthesis, which prevents them from presenting newly encountered Ags. DCs can also be indirectly activated by inflammatory mediators released during infection (e.g., IFN). Indirectly activated DCs mature but do not present pathogen Ags (as they have not encountered the pathogen) and do not provide signal 3. Therefore, although they are probably generated in large numbers upon infection or vaccination, indirectly activated DCs are considered to play little or no role in T cell immunity. In this article, we show that indirectly activated DCs retain their capacity to present Ags encountered after maturation in vivo. They can also respond to PAMPs, but the previous encounter of inflammatory signals alters their cytokine (signal 3) secretion pattern. This implies that the immune response elicited by a PAMP is more complex than predicted by the examination of the immunogenic features of directly activated DCs, and that underlying inflammatory processes can skew the immune response against pathogens. Our observations have important implications for the design of vaccines and for the understanding of the interactions between simultaneous infections, or of infection in the context of ongoing sterile inflammation.
DOI: 10.4049/jimmunol.1303215
PubMed: 25200952
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knockout</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Dendritic cells (DCs) are directly activated by pathogen-associated molecular patterns (PAMPs) and undergo maturation. Mature DCs express high levels of MHC class II molecules ("signal 1"), upregulate T cell costimulatory receptors ("signal 2"), and secrete "signal 3" cytokines (e.g., IL-12). Mature DCs efficiently present Ags linked to the activating PAMP and prime naive T cells. However, mature DCs downregulate MHC II synthesis, which prevents them from presenting newly encountered Ags. DCs can also be indirectly activated by inflammatory mediators released during infection (e.g., IFN). Indirectly activated DCs mature but do not present pathogen Ags (as they have not encountered the pathogen) and do not provide signal 3. Therefore, although they are probably generated in large numbers upon infection or vaccination, indirectly activated DCs are considered to play little or no role in T cell immunity. In this article, we show that indirectly activated DCs retain their capacity to present Ags encountered after maturation in vivo. They can also respond to PAMPs, but the previous encounter of inflammatory signals alters their cytokine (signal 3) secretion pattern. This implies that the immune response elicited by a PAMP is more complex than predicted by the examination of the immunogenic features of directly activated DCs, and that underlying inflammatory processes can skew the immune response against pathogens. Our observations have important implications for the design of vaccines and for the understanding of the interactions between simultaneous infections, or of infection in the context of ongoing sterile inflammation.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25200952</PMID><DateCreated><Year>2014</Year><Month>10</Month><Day>04</Day></DateCreated><DateCompleted><Year>2015</Year><Month>01</Month><Day>07</Day></DateCompleted><DateRevised><Year>2017</Year><Month>11</Month><Day>16</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1550-6606</ISSN><JournalIssue CitedMedium="Internet"><Volume>193</Volume><Issue>8</Issue><PubDate><Year>2014</Year><Month>Oct</Month><Day>15</Day></PubDate></JournalIssue><Title>Journal of immunology (Baltimore, Md. : 1950)</Title><ISOAbbreviation>J. Immunol.</ISOAbbreviation></Journal><ArticleTitle>Inflammation conditions mature dendritic cells to retain the capacity to present new antigens but with altered cytokine secretion function.</ArticleTitle><Pagination><MedlinePgn>3851-9</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.4049/jimmunol.1303215</ELocationID><Abstract><AbstractText>Dendritic cells (DCs) are directly activated by pathogen-associated molecular patterns (PAMPs) and undergo maturation. Mature DCs express high levels of MHC class II molecules ("signal 1"), upregulate T cell costimulatory receptors ("signal 2"), and secrete "signal 3" cytokines (e.g., IL-12). Mature DCs efficiently present Ags linked to the activating PAMP and prime naive T cells. However, mature DCs downregulate MHC II synthesis, which prevents them from presenting newly encountered Ags. DCs can also be indirectly activated by inflammatory mediators released during infection (e.g., IFN). Indirectly activated DCs mature but do not present pathogen Ags (as they have not encountered the pathogen) and do not provide signal 3. Therefore, although they are probably generated in large numbers upon infection or vaccination, indirectly activated DCs are considered to play little or no role in T cell immunity. In this article, we show that indirectly activated DCs retain their capacity to present Ags encountered after maturation in vivo. They can also respond to PAMPs, but the previous encounter of inflammatory signals alters their cytokine (signal 3) secretion pattern. This implies that the immune response elicited by a PAMP is more complex than predicted by the examination of the immunogenic features of directly activated DCs, and that underlying inflammatory processes can skew the immune response against pathogens. Our observations have important implications for the design of vaccines and for the understanding of the interactions between simultaneous infections, or of infection in the context of ongoing sterile inflammation.</AbstractText><CopyrightInformation>Copyright © 2014 by The American Association of Immunologists, Inc.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Vega-Ramos</LastName><ForeName>Javier</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, Doherty Institute of Infection and Immunity, University of Melbourne, Parkville, Victoria 3010, Australia; Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, Australia;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Roquilly</LastName><ForeName>Antoine</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, Doherty Institute of Infection and Immunity, University of Melbourne, Parkville, Victoria 3010, Australia; Surgical Intensive Care Unit, Hotel Dieu, University Hospital of Nantes, 44093 Nantes, France; and.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhan</LastName><ForeName>Yifan</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, Australia;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Young</LastName><ForeName>Louise J</ForeName><Initials>LJ</Initials><AffiliationInfo><Affiliation>Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, Australia;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mintern</LastName><ForeName>Justine D</ForeName><Initials>JD</Initials><AffiliationInfo><Affiliation>Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, Australia; Department of Biochemistry and Molecular Biology, Bio21 Molecular Science and Biotechnology Institute, University of Melbourne, Parkville, Victoria 3010, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Villadangos</LastName><ForeName>Jose A</ForeName><Initials>JA</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, Doherty Institute of Infection and Immunity, University of Melbourne, Parkville, Victoria 3010, Australia; Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, Australia; Department of Biochemistry and Molecular Biology, Bio21 Molecular Science and Biotechnology Institute, University of Melbourne, Parkville, Victoria 3010, Australia j.villadangos@unimelb.edu.au.</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>09</Month><Day>08</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">Antigens, CD8</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016207">Cytokines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000949">Histocompatibility Antigens Class II</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018836">Inflammation Mediators</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C495370">Tlr9 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051217">Toll-Like Receptor 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PubStatus="entrez"><Year>2014</Year><Month>9</Month><Day>10</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2014</Year><Month>9</Month><Day>10</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2015</Year><Month>1</Month><Day>8</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">25200952</ArticleId><ArticleId IdType="pii">jimmunol.1303215</ArticleId><ArticleId IdType="doi">10.4049/jimmunol.1303215</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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