Functional macroautophagy induction by influenza A virus without a contribution to major histocompatibility complex class II-restricted presentation.
Identifieur interne : 000C61 ( Main/Exploration ); précédent : 000C60; suivant : 000C62Functional macroautophagy induction by influenza A virus without a contribution to major histocompatibility complex class II-restricted presentation.
Auteurs : Joseph D. Comber [États-Unis] ; Tara M. Robinson ; Nicholas A. Siciliano ; Adam E. Snook ; Laurence C. EisenlohrSource :
- Journal of virology [ 1098-5514 ] ; 2011.
Descripteurs français
- KwdFr :
- Animaux, Antigènes d'histocompatibilité de classe II (métabolisme), Autophagie (immunologie), Autophagie (physiologie), Cellules dendritiques (immunologie), Femelle, Fibroblastes (physiologie), Fibroblastes (virologie), Lymphocytes T CD4+ (immunologie), Présentation d'antigène (immunologie), Souris, Souris de lignée BALB C, Sous-type H1N1 du virus de la grippe A (immunologie), Sous-type H1N1 du virus de la grippe A (pathogénicité), Sous-type H2N2 du virus de la grippe A (immunologie), Sous-type H2N2 du virus de la grippe A (pathogénicité), Test ELISpot.
- MESH :
- immunologie : Autophagie, Cellules dendritiques, Lymphocytes T CD4+, Présentation d'antigène, Sous-type H1N1 du virus de la grippe A, Sous-type H2N2 du virus de la grippe A.
- métabolisme : Antigènes d'histocompatibilité de classe II.
- pathogénicité : Sous-type H1N1 du virus de la grippe A, Sous-type H2N2 du virus de la grippe A.
- physiologie : Autophagie, Fibroblastes.
- virologie : Fibroblastes.
- Animaux, Femelle, Souris, Souris de lignée BALB C, Test ELISpot.
English descriptors
- KwdEn :
- Animals, Antigen Presentation (immunology), Autophagy (immunology), Autophagy (physiology), CD4-Positive T-Lymphocytes (immunology), Dendritic Cells (immunology), Enzyme-Linked Immunospot Assay, Female, Fibroblasts (physiology), Fibroblasts (virology), Histocompatibility Antigens Class II (metabolism), Influenza A Virus, H1N1 Subtype (immunology), Influenza A Virus, H1N1 Subtype (pathogenicity), Influenza A Virus, H2N2 Subtype (immunology), Influenza A Virus, H2N2 Subtype (pathogenicity), L Cells, Mice, Mice, Inbred BALB C.
- MESH :
- chemical , metabolism : Histocompatibility Antigens Class II.
- immunology : Antigen Presentation, Autophagy, CD4-Positive T-Lymphocytes, Dendritic Cells, Influenza A Virus, H1N1 Subtype, Influenza A Virus, H2N2 Subtype.
- pathogenicity : Influenza A Virus, H1N1 Subtype, Influenza A Virus, H2N2 Subtype.
- physiology : Autophagy, Fibroblasts.
- virology : Fibroblasts.
- Animals, Enzyme-Linked Immunospot Assay, Female, L Cells, Mice, Mice, Inbred BALB C.
Abstract
Major histocompatibility complex (MHC) class II-presented peptides can be derived from both exogenous (extracellular) and endogenous (biosynthesized) sources of antigen. Although several endogenous antigen-processing pathways have been reported, little is known about their relative contributions to global CD4(+) T cell responses against complex antigens. Using influenza virus for this purpose, we assessed the role of macroautophagy, a process in which cytosolic proteins are delivered to the lysosome by de novo vesicle formation and membrane fusion. Influenza infection triggered productive macroautophagy, and autophagy-dependent presentation was readily observed with model antigens that naturally traffic to the autophagosome. Furthermore, treatments that enhance or inhibit macroautophagy modulated the level of presentation from these model antigens. However, validated enzyme-linked immunospot (ELISpot) assays of influenza-specific CD4(+) T cells from infected mice using a variety of antigen-presenting cells, including primary dendritic cells, revealed no detectable macroautophagy-dependent component. In contrast, the contribution of proteasome-dependent endogenous antigen processing to the global influenza CD4(+) response was readily appreciated. The contribution of macroautophagy to the MHC class II-restricted response may vary depending upon the pathogen.
DOI: 10.1128/JVI.02122-10
PubMed: 21525345
Affiliations:
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Le document en format XML
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Comber</name><affiliation wicri:level="1"><nlm:affiliation>Thomas Jefferson University, BLSB Room 730, Philadelphia, PA 19107, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Thomas Jefferson University, BLSB Room 730, Philadelphia, PA 19107</wicri:regionArea><wicri:noRegion>PA 19107</wicri:noRegion></affiliation></author><author><name sortKey="Robinson, Tara M" sort="Robinson, Tara M" uniqKey="Robinson T" first="Tara M" last="Robinson">Tara M. Robinson</name></author><author><name sortKey="Siciliano, Nicholas A" sort="Siciliano, Nicholas A" uniqKey="Siciliano N" first="Nicholas A" last="Siciliano">Nicholas A. Siciliano</name></author><author><name sortKey="Snook, Adam E" sort="Snook, Adam E" uniqKey="Snook A" first="Adam E" last="Snook">Adam E. Snook</name></author><author><name sortKey="Eisenlohr, Laurence C" sort="Eisenlohr, Laurence C" uniqKey="Eisenlohr L" first="Laurence C" last="Eisenlohr">Laurence C. Eisenlohr</name></author></analytic><series><title level="j">Journal of virology</title><idno type="eISSN">1098-5514</idno><imprint><date when="2011" type="published">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Antigen Presentation (immunology)</term><term>Autophagy (immunology)</term><term>Autophagy (physiology)</term><term>CD4-Positive T-Lymphocytes (immunology)</term><term>Dendritic Cells (immunology)</term><term>Enzyme-Linked Immunospot Assay</term><term>Female</term><term>Fibroblasts (physiology)</term><term>Fibroblasts (virology)</term><term>Histocompatibility Antigens Class II (metabolism)</term><term>Influenza A Virus, H1N1 Subtype (immunology)</term><term>Influenza A Virus, H1N1 Subtype (pathogenicity)</term><term>Influenza A Virus, H2N2 Subtype (immunology)</term><term>Influenza A Virus, H2N2 Subtype (pathogenicity)</term><term>L Cells</term><term>Mice</term><term>Mice, Inbred BALB C</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Antigènes d'histocompatibilité de classe II (métabolisme)</term><term>Autophagie (immunologie)</term><term>Autophagie (physiologie)</term><term>Cellules dendritiques (immunologie)</term><term>Femelle</term><term>Fibroblastes (physiologie)</term><term>Fibroblastes (virologie)</term><term>Lymphocytes T CD4+ (immunologie)</term><term>Présentation d'antigène (immunologie)</term><term>Souris</term><term>Souris de lignée BALB C</term><term>Sous-type H1N1 du virus de la grippe A (immunologie)</term><term>Sous-type H1N1 du virus de la grippe A (pathogénicité)</term><term>Sous-type H2N2 du virus de la grippe A (immunologie)</term><term>Sous-type H2N2 du virus de la grippe A (pathogénicité)</term><term>Test ELISpot</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Histocompatibility Antigens Class II</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Autophagie</term><term>Cellules dendritiques</term><term>Lymphocytes T CD4+</term><term>Présentation d'antigène</term><term>Sous-type H1N1 du virus de la grippe A</term><term>Sous-type H2N2 du virus de la grippe A</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Antigen Presentation</term><term>Autophagy</term><term>CD4-Positive T-Lymphocytes</term><term>Dendritic Cells</term><term>Influenza A Virus, H1N1 Subtype</term><term>Influenza A Virus, H2N2 Subtype</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Antigènes d'histocompatibilité de classe II</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Influenza A Virus, H1N1 Subtype</term><term>Influenza A Virus, H2N2 Subtype</term></keywords><keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Sous-type H1N1 du virus de la grippe A</term><term>Sous-type H2N2 du virus de la grippe A</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Autophagie</term><term>Fibroblastes</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Autophagy</term><term>Fibroblasts</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Fibroblastes</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Fibroblasts</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Enzyme-Linked Immunospot Assay</term><term>Female</term><term>L Cells</term><term>Mice</term><term>Mice, Inbred BALB C</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Femelle</term><term>Souris</term><term>Souris de lignée BALB C</term><term>Test ELISpot</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Major histocompatibility complex (MHC) class II-presented peptides can be derived from both exogenous (extracellular) and endogenous (biosynthesized) sources of antigen. Although several endogenous antigen-processing pathways have been reported, little is known about their relative contributions to global CD4(+) T cell responses against complex antigens. Using influenza virus for this purpose, we assessed the role of macroautophagy, a process in which cytosolic proteins are delivered to the lysosome by de novo vesicle formation and membrane fusion. Influenza infection triggered productive macroautophagy, and autophagy-dependent presentation was readily observed with model antigens that naturally traffic to the autophagosome. Furthermore, treatments that enhance or inhibit macroautophagy modulated the level of presentation from these model antigens. However, validated enzyme-linked immunospot (ELISpot) assays of influenza-specific CD4(+) T cells from infected mice using a variety of antigen-presenting cells, including primary dendritic cells, revealed no detectable macroautophagy-dependent component. In contrast, the contribution of proteasome-dependent endogenous antigen processing to the global influenza CD4(+) response was readily appreciated. The contribution of macroautophagy to the MHC class II-restricted response may vary depending upon the pathogen.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country></list><tree><noCountry><name sortKey="Eisenlohr, Laurence C" sort="Eisenlohr, Laurence C" uniqKey="Eisenlohr L" first="Laurence C" last="Eisenlohr">Laurence C. Eisenlohr</name><name sortKey="Robinson, Tara M" sort="Robinson, Tara M" uniqKey="Robinson T" first="Tara M" last="Robinson">Tara M. Robinson</name><name sortKey="Siciliano, Nicholas A" sort="Siciliano, Nicholas A" uniqKey="Siciliano N" first="Nicholas A" last="Siciliano">Nicholas A. Siciliano</name><name sortKey="Snook, Adam E" sort="Snook, Adam E" uniqKey="Snook A" first="Adam E" last="Snook">Adam E. Snook</name></noCountry><country name="États-Unis"><noRegion><name sortKey="Comber, Joseph D" sort="Comber, Joseph D" uniqKey="Comber J" first="Joseph D" last="Comber">Joseph D. Comber</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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