The Tumor Antigen NY-ESO-1 Mediates Direct Recognition of Melanoma Cells by CD4+ T Cells after Intercellular Antigen Transfer.
Identifieur interne : 002521 ( PubMed/Corpus ); précédent : 002520; suivant : 002522The Tumor Antigen NY-ESO-1 Mediates Direct Recognition of Melanoma Cells by CD4+ T Cells after Intercellular Antigen Transfer.
Auteurs : Jean Francois Fonteneau ; Fabienne Brilot ; Christian Münz ; Monique GannagéSource :
- Journal of immunology (Baltimore, Md. : 1950) [ 1550-6606 ] ; 2016.
English descriptors
- KwdEn :
- Acetylcysteine (analogs & derivatives), Acetylcysteine (pharmacology), Antigen Presentation (immunology), Antigens, Neoplasm (immunology), Autophagy (immunology), Autophagy-Related Protein 12, CD4-Positive T-Lymphocytes (immunology), CD4-Positive T-Lymphocytes (transplantation), Cell Line, Tumor, Chloroquine (pharmacology), Dendritic Cells (immunology), Endocytosis (immunology), Epitopes, T-Lymphocyte (immunology), Histocompatibility Antigens Class II (immunology), Humans, Immunotherapy, Adoptive, Leupeptins, Lymphocyte Activation (immunology), Lysosomal-Associated Membrane Protein 2 (genetics), Melanoma (immunology), Melanoma (therapy), Membrane Proteins (immunology), RNA Interference, RNA, Small Interfering, Small Ubiquitin-Related Modifier Proteins (genetics).
- MESH :
- chemical , analogs & derivatives : Acetylcysteine.
- chemical , genetics : Lysosomal-Associated Membrane Protein 2, Small Ubiquitin-Related Modifier Proteins.
- chemical , immunology : Antigens, Neoplasm, Epitopes, T-Lymphocyte, Histocompatibility Antigens Class II, Membrane Proteins.
- chemical , pharmacology : Acetylcysteine, Chloroquine.
- immunology : Antigen Presentation, Autophagy, CD4-Positive T-Lymphocytes, Dendritic Cells, Endocytosis, Lymphocyte Activation, Melanoma.
- therapy : Melanoma.
- transplantation : CD4-Positive T-Lymphocytes.
- chemical : Autophagy-Related Protein 12, Cell Line, Tumor, Humans, Immunotherapy, Adoptive, Leupeptins, RNA Interference, RNA, Small Interfering.
Abstract
NY-ESO-1-specific CD4(+) T cells are of interest for immune therapy against tumors, because it has been shown that their transfer into a patient with melanoma resulted in tumor regression. Therefore, we investigated how NY-ESO-1 is processed onto MHC class II molecules for direct CD4(+) T cell recognition of melanoma cells. We could rule out proteasome and autophagy-dependent endogenous Ag processing for MHC class II presentation. In contrast, intercellular Ag transfer, followed by classical MHC class II Ag processing via endocytosis, sensitized neighboring melanoma cells for CD4(+) T cell recognition. However, macroautophagy targeting of NY-ESO-1 enhanced MHC class II presentation. Therefore, both elevated NY-ESO-1 release and macroautophagy targeting could improve melanoma cell recognition by CD4(+) T cells and should be explored during immunotherapy of melanoma.
DOI: 10.4049/jimmunol.1402664
PubMed: 26608910
Links to Exploration step
pubmed:26608910Le document en format XML
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Department of Pathology and Immunology, School of Medicine, University of Geneva, Geneva 1211, Switzerland; and Division of Rheumatology, Department of Internal Medicine, University Hospital, Geneva 1205, Switzerland monique.ghannage@unige.ch.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2016">2016</date><idno type="RBID">pubmed:26608910</idno><idno type="pmid">26608910</idno><idno type="doi">10.4049/jimmunol.1402664</idno><idno type="wicri:Area/PubMed/Corpus">002521</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">002521</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">The Tumor Antigen NY-ESO-1 Mediates Direct Recognition of Melanoma Cells by CD4+ T Cells after Intercellular Antigen Transfer.</title><author><name sortKey="Fonteneau, Jean Francois" sort="Fonteneau, Jean Francois" uniqKey="Fonteneau J" first="Jean Francois" last="Fonteneau">Jean Francois Fonteneau</name><affiliation><nlm:affiliation>INSERM UMR892, CNRS UMR6299, Université de Nantes, Nantes 44007, France;</nlm:affiliation></affiliation></author><author><name sortKey="Brilot, Fabienne" sort="Brilot, Fabienne" uniqKey="Brilot F" first="Fabienne" last="Brilot">Fabienne Brilot</name><affiliation><nlm:affiliation>Neuroimmunology Group, Institute for Neuroscience and Muscle Research, The Kids Research Institute at the Children's Hospital at Westmead, St. Westmead, New South Wales 2145, Australia;</nlm:affiliation></affiliation></author><author><name sortKey="Munz, Christian" sort="Munz, Christian" uniqKey="Munz C" first="Christian" last="Münz">Christian Münz</name><affiliation><nlm:affiliation>Viral Immunobiology, Institute of Experimental Immunology, University of Zürich, Zürich 8006, Switzerland;</nlm:affiliation></affiliation></author><author><name sortKey="Gannage, Monique" sort="Gannage, Monique" uniqKey="Gannage M" first="Monique" last="Gannagé">Monique Gannagé</name><affiliation><nlm:affiliation>Viral Immunobiology, Institute of Experimental Immunology, University of Zürich, Zürich 8006, Switzerland; Department of Pathology and Immunology, School of Medicine, University of Geneva, Geneva 1211, Switzerland; and Division of Rheumatology, Department of Internal Medicine, University Hospital, Geneva 1205, Switzerland monique.ghannage@unige.ch.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Journal of immunology (Baltimore, Md. : 1950)</title><idno type="eISSN">1550-6606</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Acetylcysteine (analogs & derivatives)</term><term>Acetylcysteine (pharmacology)</term><term>Antigen Presentation (immunology)</term><term>Antigens, Neoplasm (immunology)</term><term>Autophagy (immunology)</term><term>Autophagy-Related Protein 12</term><term>CD4-Positive T-Lymphocytes (immunology)</term><term>CD4-Positive T-Lymphocytes (transplantation)</term><term>Cell Line, Tumor</term><term>Chloroquine (pharmacology)</term><term>Dendritic Cells (immunology)</term><term>Endocytosis (immunology)</term><term>Epitopes, T-Lymphocyte (immunology)</term><term>Histocompatibility Antigens Class II (immunology)</term><term>Humans</term><term>Immunotherapy, Adoptive</term><term>Leupeptins</term><term>Lymphocyte Activation (immunology)</term><term>Lysosomal-Associated Membrane Protein 2 (genetics)</term><term>Melanoma (immunology)</term><term>Melanoma (therapy)</term><term>Membrane Proteins (immunology)</term><term>RNA Interference</term><term>RNA, Small Interfering</term><term>Small Ubiquitin-Related Modifier Proteins (genetics)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Acetylcysteine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Lysosomal-Associated Membrane Protein 2</term><term>Small Ubiquitin-Related Modifier Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Antigens, Neoplasm</term><term>Epitopes, T-Lymphocyte</term><term>Histocompatibility Antigens Class II</term><term>Membrane Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Acetylcysteine</term><term>Chloroquine</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>Endocytosis</term><term>Lymphocyte Activation</term><term>Melanoma</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Melanoma</term></keywords><keywords scheme="MESH" qualifier="transplantation" xml:lang="en"><term>CD4-Positive T-Lymphocytes</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Autophagy-Related Protein 12</term><term>Cell Line, Tumor</term><term>Humans</term><term>Immunotherapy, Adoptive</term><term>Leupeptins</term><term>RNA Interference</term><term>RNA, Small Interfering</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">NY-ESO-1-specific CD4(+) T cells are of interest for immune therapy against tumors, because it has been shown that their transfer into a patient with melanoma resulted in tumor regression. Therefore, we investigated how NY-ESO-1 is processed onto MHC class II molecules for direct CD4(+) T cell recognition of melanoma cells. We could rule out proteasome and autophagy-dependent endogenous Ag processing for MHC class II presentation. In contrast, intercellular Ag transfer, followed by classical MHC class II Ag processing via endocytosis, sensitized neighboring melanoma cells for CD4(+) T cell recognition. However, macroautophagy targeting of NY-ESO-1 enhanced MHC class II presentation. Therefore, both elevated NY-ESO-1 release and macroautophagy targeting could improve melanoma cell recognition by CD4(+) T cells and should be explored during immunotherapy of melanoma.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26608910</PMID><DateCreated><Year>2015</Year><Month>12</Month><Day>19</Day></DateCreated><DateCompleted><Year>2016</Year><Month>05</Month><Day>24</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>26</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1550-6606</ISSN><JournalIssue CitedMedium="Internet"><Volume>196</Volume><Issue>1</Issue><PubDate><Year>2016</Year><Month>Jan</Month><Day>01</Day></PubDate></JournalIssue><Title>Journal of immunology (Baltimore, Md. : 1950)</Title><ISOAbbreviation>J. Immunol.</ISOAbbreviation></Journal><ArticleTitle>The Tumor Antigen NY-ESO-1 Mediates Direct Recognition of Melanoma Cells by CD4+ T Cells after Intercellular Antigen Transfer.</ArticleTitle><Pagination><MedlinePgn>64-71</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.4049/jimmunol.1402664</ELocationID><Abstract><AbstractText>NY-ESO-1-specific CD4(+) T cells are of interest for immune therapy against tumors, because it has been shown that their transfer into a patient with melanoma resulted in tumor regression. Therefore, we investigated how NY-ESO-1 is processed onto MHC class II molecules for direct CD4(+) T cell recognition of melanoma cells. We could rule out proteasome and autophagy-dependent endogenous Ag processing for MHC class II presentation. In contrast, intercellular Ag transfer, followed by classical MHC class II Ag processing via endocytosis, sensitized neighboring melanoma cells for CD4(+) T cell recognition. However, macroautophagy targeting of NY-ESO-1 enhanced MHC class II presentation. Therefore, both elevated NY-ESO-1 release and macroautophagy targeting could improve melanoma cell recognition by CD4(+) T cells and should be explored during immunotherapy of melanoma.</AbstractText><CopyrightInformation>Copyright © 2015 by The American Association of Immunologists, Inc.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Fonteneau</LastName><ForeName>Jean Francois</ForeName><Initials>JF</Initials><Identifier Source="ORCID">http://orcid.org/0000-0002-3284-8319</Identifier><AffiliationInfo><Affiliation>INSERM UMR892, CNRS UMR6299, Université de Nantes, Nantes 44007, France;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Brilot</LastName><ForeName>Fabienne</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Neuroimmunology Group, Institute for Neuroscience and Muscle Research, The Kids Research Institute at the Children's Hospital at Westmead, St. Westmead, New South Wales 2145, Australia;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Münz</LastName><ForeName>Christian</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Viral Immunobiology, Institute of Experimental Immunology, University of Zürich, Zürich 8006, Switzerland;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gannagé</LastName><ForeName>Monique</ForeName><Initials>M</Initials><Identifier Source="ORCID">http://orcid.org/0000-0003-3533-1937</Identifier><AffiliationInfo><Affiliation>Viral Immunobiology, Institute of Experimental Immunology, University of Zürich, Zürich 8006, Switzerland; Department of Pathology and Immunology, School of Medicine, University of Geneva, Geneva 1211, Switzerland; and Division of Rheumatology, Department of Internal Medicine, University Hospital, Geneva 1205, Switzerland monique.ghannage@unige.ch.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList 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Source="NLM">PMC4683358</OtherID></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2014</Year><Month>10</Month><Day>21</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2015</Year><Month>10</Month><Day>13</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2015</Year><Month>11</Month><Day>27</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2015</Year><Month>11</Month><Day>27</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2016</Year><Month>5</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">26608910</ArticleId><ArticleId IdType="pii">jimmunol.1402664</ArticleId><ArticleId IdType="doi">10.4049/jimmunol.1402664</ArticleId><ArticleId IdType="pmc">PMC4683358</ArticleId><ArticleId 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