Tumour-specific MHC-class-II-restricted responses after in vitro sensitization to synthetic peptides corresponding to gp100 and Annexin II eluted from melanoma cells
Identifieur interne : 003B09 ( Main/Exploration ); précédent : 003B08; suivant : 003B10Tumour-specific MHC-class-II-restricted responses after in vitro sensitization to synthetic peptides corresponding to gp100 and Annexin II eluted from melanoma cells
Auteurs : Kun Li [États-Unis] ; Medi Adibzadeh [États-Unis] ; Thomas Halder [États-Unis] ; Hubert Kalbacher [États-Unis] ; Susanne Heinzel [États-Unis] ; Claudia Müller [États-Unis] ; Jesper Zeuthen ; Graham Pawelec [États-Unis]Source :
- Cancer Immunology, Immunotherapy [ 0340-7004 ] ; 1998-08-01.
Descripteurs français
- KwdFr :
- Animaux, Annexine A2 (immunologie), Anticorps antitumoraux (immunologie), Antigène gp100 du mélanome, Antigènes d'histocompatibilité de classe II (pharmacologie), Cellules CHO (métabolisme), Cellules cancéreuses en culture, Cricetinae, Fragments peptidiques (biosynthèse), Glycoprotéines membranaires (immunologie), Humains, Immunisation, Mélanome expérimental (anatomopathologie), Mélanome expérimental (immunologie), Protéines tumorales (immunologie), Spécificité des anticorps.
- MESH :
- anatomopathologie : Mélanome expérimental.
- biosynthèse : Fragments peptidiques.
- immunologie : Annexine A2, Anticorps antitumoraux, Glycoprotéines membranaires, Mélanome expérimental, Protéines tumorales.
- métabolisme : Cellules CHO.
- pharmacologie : Antigènes d'histocompatibilité de classe II.
- Animaux, Antigène gp100 du mélanome, Cellules cancéreuses en culture, Cricetinae, Humains, Immunisation, Spécificité des anticorps.
English descriptors
- KwdEn :
- Animals, Annexin A2 (immunology), Antibodies, Neoplasm (immunology), Antibody Specificity, Apoptosis, CHO Cells (metabolism), Cricetinae, Histocompatibility Antigens Class II (pharmacology), Humans, Immunization, Key words HLA-DR-restricted tumour antigens, Melanoma, Melanoma, Experimental (immunology), Melanoma, Experimental (pathology), Membrane Glycoproteins (immunology), Neoplasm Proteins (immunology), Peptide Fragments (biosynthesis), Synthetic peptide antigens, Tumor Cells, Cultured, Tumour escape from immune responses, gp100 Melanoma Antigen.
- MESH :
- chemical , biosynthesis : Peptide Fragments.
- chemical , immunology : Annexin A2, Antibodies, Neoplasm, Membrane Glycoproteins, Neoplasm Proteins.
- immunology : Melanoma, Experimental.
- metabolism : CHO Cells.
- pathology : Melanoma, Experimental.
- chemical , pharmacology : Histocompatibility Antigens Class II.
- Animals, Antibody Specificity, Cricetinae, Humans, Immunization, Tumor Cells, Cultured, gp100 Melanoma Antigen.
Abstract
Abstract: In a search for potentially tumour-specific MHC-class-II-restricted antigens, the immunogenicity of endogenous peptides that had been eluted from HLA-DR molecules of the human melanoma cell line FM3 (HLA-DRB1*02x, DRB1*0401) was tested in vitro. Two 16-mers representing gp100 positions 44–59, and annexin II positions 208–223 bound well to isolated DRB1*0401 molecules and are discussed here. HLA-DR-matched normal donors' T cells were cultured with peptide-pulsed artificial antigen-presenting cells (CHO cells cotransfected with genes for HLA-DRB1*0401 and CD80 and coexpressing high levels of both human molecules). Specific sensitization was achieved against both peptides, as measured in assays of autocrine proliferation and interleukin-2 secretion. Moreover, responses to native autologous melanoma cells but not to autologous B cells were also observed. In view of the expression of fas by the activated T cells and of fas ligand by the melanoma cells, blockade of potential fas/fas-ligand interactions was undertaken using monoclonal antibodies (mAb). The antagonistic fas-specific mAb M3, but not the fas agonist M33, caused a markedly enhanced T cell response to FM3 cells. These results demonstrate that synthetic peptide antigens are able to sensitize T cells in vitro for effective MHC-class-II-restricted recognition of melanoma cells.
Url:
DOI: 10.1007/s002620050501
Affiliations:
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type="state">Delaware</region></placeName><wicri:cityArea>Tübingen Ageing and Tumour Immunology Group, University of Tübingen Center for Medical Research, Derendingen, Tübingen, Germany</wicri:cityArea></affiliation></author><author><name sortKey="Halder, Thomas" sort="Halder, Thomas" uniqKey="Halder T" first="Thomas" last="Halder">Thomas Halder</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Delaware</region></placeName><wicri:cityArea>Medical and Natural Sciences Research Center, University of Tübingen, Tübingen, Germany</wicri:cityArea></affiliation></author><author><name sortKey="Kalbacher, Hubert" sort="Kalbacher, Hubert" uniqKey="Kalbacher H" first="Hubert" last="Kalbacher">Hubert Kalbacher</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Delaware</region></placeName><wicri:cityArea>Medical and Natural Sciences Research Center, University of Tübingen, 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type="eISSN">1432-0851</idno><imprint><publisher>Springer-Verlag</publisher><pubPlace>Berlin/Heidelberg</pubPlace><date type="published" when="1998-08-01">1998-08-01</date><biblScope unit="volume">47</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="32">32</biblScope><biblScope unit="page" to="38">38</biblScope></imprint><idno type="ISSN">0340-7004</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0340-7004</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Annexin A2 (immunology)</term><term>Antibodies, Neoplasm (immunology)</term><term>Antibody Specificity</term><term>Apoptosis</term><term>CHO Cells (metabolism)</term><term>Cricetinae</term><term>Histocompatibility Antigens Class II (pharmacology)</term><term>Humans</term><term>Immunization</term><term>Key words HLA-DR-restricted tumour antigens</term><term>Melanoma</term><term>Melanoma, Experimental (immunology)</term><term>Melanoma, Experimental (pathology)</term><term>Membrane Glycoproteins (immunology)</term><term>Neoplasm Proteins (immunology)</term><term>Peptide Fragments (biosynthesis)</term><term>Synthetic peptide antigens</term><term>Tumor Cells, Cultured</term><term>Tumour escape from immune responses</term><term>gp100 Melanoma Antigen</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Annexine A2 (immunologie)</term><term>Anticorps antitumoraux (immunologie)</term><term>Antigène gp100 du mélanome</term><term>Antigènes d'histocompatibilité de classe II (pharmacologie)</term><term>Cellules CHO (métabolisme)</term><term>Cellules cancéreuses en culture</term><term>Cricetinae</term><term>Fragments peptidiques (biosynthèse)</term><term>Glycoprotéines membranaires (immunologie)</term><term>Humains</term><term>Immunisation</term><term>Mélanome expérimental (anatomopathologie)</term><term>Mélanome expérimental (immunologie)</term><term>Protéines tumorales (immunologie)</term><term>Spécificité des anticorps</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Peptide Fragments</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Annexin A2</term><term>Antibodies, Neoplasm</term><term>Membrane Glycoproteins</term><term>Neoplasm Proteins</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Mélanome expérimental</term></keywords><keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Fragments peptidiques</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Annexine A2</term><term>Anticorps antitumoraux</term><term>Glycoprotéines membranaires</term><term>Mélanome expérimental</term><term>Protéines tumorales</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Melanoma, Experimental</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>CHO Cells</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cellules CHO</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Melanoma, Experimental</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Antigènes d'histocompatibilité de classe II</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Histocompatibility Antigens Class II</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Antibody Specificity</term><term>Cricetinae</term><term>Humans</term><term>Immunization</term><term>Tumor Cells, Cultured</term><term>gp100 Melanoma Antigen</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Antigène gp100 du mélanome</term><term>Cellules cancéreuses en culture</term><term>Cricetinae</term><term>Humains</term><term>Immunisation</term><term>Spécificité des anticorps</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: In a search for potentially tumour-specific MHC-class-II-restricted antigens, the immunogenicity of endogenous peptides that had been eluted from HLA-DR molecules of the human melanoma cell line FM3 (HLA-DRB1*02x, DRB1*0401) was tested in vitro. Two 16-mers representing gp100 positions 44–59, and annexin II positions 208–223 bound well to isolated DRB1*0401 molecules and are discussed here. HLA-DR-matched normal donors' T cells were cultured with peptide-pulsed artificial antigen-presenting cells (CHO cells cotransfected with genes for HLA-DRB1*0401 and CD80 and coexpressing high levels of both human molecules). Specific sensitization was achieved against both peptides, as measured in assays of autocrine proliferation and interleukin-2 secretion. Moreover, responses to native autologous melanoma cells but not to autologous B cells were also observed. In view of the expression of fas by the activated T cells and of fas ligand by the melanoma cells, blockade of potential fas/fas-ligand interactions was undertaken using monoclonal antibodies (mAb). The antagonistic fas-specific mAb M3, but not the fas agonist M33, caused a markedly enhanced T cell response to FM3 cells. These results demonstrate that synthetic peptide antigens are able to sensitize T cells in vitro for effective MHC-class-II-restricted recognition of melanoma cells.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Delaware</li></region></list><tree><noCountry><name sortKey="Zeuthen, Jesper" sort="Zeuthen, Jesper" uniqKey="Zeuthen J" first="Jesper" last="Zeuthen">Jesper Zeuthen</name></noCountry><country name="États-Unis"><region name="Delaware"><name sortKey="Li, Kun" sort="Li, Kun" uniqKey="Li K" first="Kun" last="Li">Kun Li</name></region><name sortKey="Adibzadeh, Medi" sort="Adibzadeh, Medi" uniqKey="Adibzadeh M" first="Medi" last="Adibzadeh">Medi Adibzadeh</name><name sortKey="Halder, Thomas" sort="Halder, Thomas" uniqKey="Halder T" first="Thomas" last="Halder">Thomas Halder</name><name sortKey="Heinzel, Susanne" sort="Heinzel, Susanne" uniqKey="Heinzel S" first="Susanne" last="Heinzel">Susanne Heinzel</name><name sortKey="Kalbacher, Hubert" sort="Kalbacher, Hubert" uniqKey="Kalbacher H" first="Hubert" last="Kalbacher">Hubert Kalbacher</name><name sortKey="Muller, Claudia" sort="Muller, Claudia" uniqKey="Muller C" first="Claudia" last="Müller">Claudia Müller</name><name sortKey="Pawelec, Graham" sort="Pawelec, Graham" uniqKey="Pawelec G" first="Graham" last="Pawelec">Graham Pawelec</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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