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 : 000386 ( Istex/Curation ); précédent : 000385; suivant : 000387Tumour-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.
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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.
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DOI: 10.1007/s002620050501
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Tübingen, Germany, DE</mods:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Delaware</region></placeName><wicri:cityArea>Section for Transplantation Immunology and Immunohaematology, Second Department of Internal Medicine, University of Tübingen Medical School, Tübingen, Germany</wicri:cityArea></affiliation></author><author><name sortKey="Adibzadeh, Medi" sort="Adibzadeh, Medi" uniqKey="Adibzadeh M" first="Medi" last="Adibzadeh">Medi Adibzadeh</name><affiliation wicri:level="2"><mods:affiliation>Tübingen Ageing and Tumour Immunology Group, University of Tübingen Center for Medical Research, Derendingen, Tübingen, Germany, DE</mods:affiliation><country xml:lang="fr">États-Unis</country><placeName><region 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 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Tübingen, Tübingen, Germany</wicri:cityArea></affiliation></author><author><name sortKey="Heinzel, Susanne" sort="Heinzel, Susanne" uniqKey="Heinzel S" first="Susanne" last="Heinzel">Susanne Heinzel</name><affiliation wicri:level="2"><mods:affiliation>Tübingen Ageing and Tumour Immunology Group, University of Tübingen Center for Medical Research, Derendingen, Tübingen, Germany, DE</mods:affiliation><country xml:lang="fr">États-Unis</country><placeName><region 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="Muller, Claudia" sort="Muller, Claudia" uniqKey="Muller C" first="Claudia" last="Müller">Claudia Müller</name><affiliation wicri:level="2"><mods:affiliation>Section for Transplantation Immunology and Immunohaematology, Second Department of Internal Medicine, University of Tübingen Medical School, Tübingen, Germany, DE</mods:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Delaware</region></placeName><wicri:cityArea>Section for Transplantation Immunology and Immunohaematology, Second Department of Internal Medicine, University of Tübingen Medical School, Tübingen, Germany</wicri:cityArea></affiliation></author><author><name sortKey="Zeuthen, Jesper" sort="Zeuthen, Jesper" uniqKey="Zeuthen J" first="Jesper" last="Zeuthen">Jesper Zeuthen</name><affiliation><mods:affiliation>Danish Cancer Society, Copenhagen, Denmark, DK</mods:affiliation><wicri:noCountry code="subField">DK</wicri:noCountry></affiliation></author><author><name sortKey="Pawelec, Graham" sort="Pawelec, Graham" uniqKey="Pawelec G" first="Graham" last="Pawelec">Graham Pawelec</name><affiliation wicri:level="2"><mods:affiliation>Tübingen Ageing and Tumour Immunology Group, University of Tübingen Center for Medical Research, Derendingen, Tübingen, Germany, DE</mods:affiliation><country xml:lang="fr">États-Unis</country><placeName><region 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></analytic><monogr></monogr><series><title level="j">Cancer Immunology, Immunotherapy</title><title level="j" type="abbrev">Cancer Immunol Immunother</title><idno type="ISSN">0340-7004</idno><idno 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>Apoptosis</term><term>Key words HLA-DR-restricted tumour antigens</term><term>Melanoma</term><term>Synthetic peptide antigens</term><term>Tumour escape from immune responses</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></record>Pour manipuler ce document sous Unix (Dilib)
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