Identification of HTLV-1-Specific CTL Directed against Synthetic and Naturally Processed Peptides in HLA-B*3501 Transgenic Mice
Identifieur interne : 003F63 ( Main/Exploration ); précédent : 003F62; suivant : 003F64Identification of HTLV-1-Specific CTL Directed against Synthetic and Naturally Processed Peptides in HLA-B*3501 Transgenic Mice
Auteurs : Christian Schönbach [Japon] ; Kiyoshi Nokihara [Japon] ; Charles R. M. Bangham [Royaume-Uni] ; Ai Kariyone [Japon] ; Sachiko Karaki [Japon] ; Hisatoshi Shida [Japon] ; Kiyoshi Takatsu [Japon] ; Kohji Egawa [Japon] ; Karl-Heinz Wiesmüller [Allemagne] ; Masafumi Takiguchi [Japon]Source :
- Virology [ 0042-6822 ] ; 1996.
English descriptors
- Teeft :
- Adjuvant, Adult leukemia, Anchor residues, Binder, Binding peptides, Binding site, Bulk cultures, Cell epitopes, Chimeric, Cytotoxic, Epitope, Fluorescence intensity, Gafltnvpy, High binders, Immunization, Immunogenicity, Immunol, Lymphocyte, Medium binders, Monoclonal antibody, Mouse, Multiple epitopes, Peptide, Peptide vpspsstpll, Present address, Qafpqctil, Qafpqctilqy, Recombinant, Recombinant vaccinia virus, Schonbach, Specific lysis, Spleen cells, Sppstplly, Takiguchi, Target cells, Transgenic, Transgenic mice, Transgenic mouse, Transgenic mouse model, Tropical spastic paraparesis, Vaccine, Vaccinia, Viral, Virology, Virology induction, Virology schonbach, Vpspsstpll, Vpspsstplly.
Abstract
Abstract: Previous studies of CTL responses to influenza peptides in HLA single transgenic mice resulted in the identification of at most one immunodominant epitope. Since HLA-B*3501 is known to present multiple HIV-1-specific T cell epitopes we tested the cellular immune response of HLA-B*3501 transgenic mice to synthetic HTLV-1 peptides mixed with the lipohexapeptideN-palmitoyl-S-[2,3-bis(palmitoyloxy)propyl]cysteinyl-seryl-lysyl-lysyl-lysyl-lysine, which is a biocompatible, Th-epitope-independent adjuvant. Eleven of 37 tested HLA-B*3501 binding peptides mounted a CTL response after threein vitrostimulations. The HLA-B*3501 affinity of peptides correlated with their ability to induce CTL in HLA-B*3501 transgenic mice. Seven peptides derived from env-gp46 (VPSPSSTPLL, VPSSSSTPL, YPSLALAPH, and YPSLALAPA), pol (QAFPQCTIL), gag-p19 (YPGRVNEIL), and tax (GAFLTNVPY) proteins induced peptide-specific CTL. Bulk CTL generated by four peptides derived from env-gp46 (SPPSTPLLY, VPSPSSTPLLY, and VPSPSSTPLL) and pol (QAFPQCTILQY) killed peptide-pulsed and recombinant vaccinia-infected target cells. The latter peptides therefore present T-cell epitopes and are vaccine candidates for our transgenic mouse model.
Url:
DOI: 10.1006/viro.1996.0632
Affiliations:
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Nakagyo-ku, Kyoto, 604</wicri:regionArea><wicri:noRegion>604</wicri:noRegion></affiliation></author><author><name sortKey="Bangham, Charles R M" sort="Bangham, Charles R M" uniqKey="Bangham C" first="Charles R. M." last="Bangham">Charles R. M. Bangham</name><affiliation wicri:level="1"><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Department of Immunology, Imperial College School of Medicine at St. Mary's, London, W2 1PG</wicri:regionArea><wicri:noRegion>W2 1PG</wicri:noRegion></affiliation></author><author><name sortKey="Kariyone, Ai" sort="Kariyone, Ai" uniqKey="Kariyone A" first="Ai" last="Kariyone">Ai Kariyone</name><affiliation wicri:level="4"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Immunology, Institute of Medical Science, University of Tokyo, Tokyo, 108</wicri:regionArea><orgName type="university">Université de Tokyo</orgName><placeName><settlement type="city">Tokyo</settlement><region type="province">Région de Kantō</region></placeName></affiliation></author><author><name sortKey="Karaki, Sachiko" sort="Karaki, Sachiko" uniqKey="Karaki S" first="Sachiko" last="Karaki">Sachiko Karaki</name><affiliation wicri:level="4"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Tumor Biology, Institute of Medical Science, University of Tokyo, Tokyo, 108</wicri:regionArea><orgName type="university">Université de Tokyo</orgName><placeName><settlement type="city">Tokyo</settlement><region type="province">Région de Kantō</region></placeName></affiliation></author><author><name sortKey="Shida, Hisatoshi" sort="Shida, Hisatoshi" uniqKey="Shida H" first="Hisatoshi" last="Shida">Hisatoshi Shida</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Institute for Virus Research, University of Kyoto, Sakyo-ku, Kyoto, 606</wicri:regionArea><wicri:noRegion>606</wicri:noRegion></affiliation></author><author><name sortKey="Takatsu, Kiyoshi" sort="Takatsu, Kiyoshi" uniqKey="Takatsu K" first="Kiyoshi" last="Takatsu">Kiyoshi Takatsu</name><affiliation wicri:level="4"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Immunology, Institute of Medical Science, 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xml:lang="fr">Allemagne</country><wicri:regionArea>Natural and Medical Science Institute, University of Tübingen, 72762, Reutlingen</wicri:regionArea><wicri:noRegion>72762, Reutlingen</wicri:noRegion><wicri:noRegion>Reutlingen</wicri:noRegion></affiliation></author><author><name sortKey="Takiguchi, Masafumi" sort="Takiguchi, Masafumi" uniqKey="Takiguchi M" first="Masafumi" last="Takiguchi">Masafumi Takiguchi</name><affiliation wicri:level="4"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Tumor Biology, Institute of Medical Science, University of Tokyo, Tokyo, 108</wicri:regionArea><orgName type="university">Université de Tokyo</orgName><placeName><settlement type="city">Tokyo</settlement><region type="province">Région de Kantō</region></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j">Virology</title><title level="j" type="abbrev">YVIRO</title><idno type="ISSN">0042-6822</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1996">1996</date><biblScope unit="volume">226</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="102">102</biblScope><biblScope unit="page" to="112">112</biblScope></imprint><idno type="ISSN">0042-6822</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0042-6822</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Adjuvant</term><term>Adult leukemia</term><term>Anchor residues</term><term>Binder</term><term>Binding peptides</term><term>Binding site</term><term>Bulk cultures</term><term>Cell epitopes</term><term>Chimeric</term><term>Cytotoxic</term><term>Epitope</term><term>Fluorescence intensity</term><term>Gafltnvpy</term><term>High binders</term><term>Immunization</term><term>Immunogenicity</term><term>Immunol</term><term>Lymphocyte</term><term>Medium binders</term><term>Monoclonal antibody</term><term>Mouse</term><term>Multiple epitopes</term><term>Peptide</term><term>Peptide vpspsstpll</term><term>Present address</term><term>Qafpqctil</term><term>Qafpqctilqy</term><term>Recombinant</term><term>Recombinant vaccinia virus</term><term>Schonbach</term><term>Specific lysis</term><term>Spleen cells</term><term>Sppstplly</term><term>Takiguchi</term><term>Target cells</term><term>Transgenic</term><term>Transgenic mice</term><term>Transgenic mouse</term><term>Transgenic mouse model</term><term>Tropical spastic paraparesis</term><term>Vaccine</term><term>Vaccinia</term><term>Viral</term><term>Virology</term><term>Virology induction</term><term>Virology schonbach</term><term>Vpspsstpll</term><term>Vpspsstplly</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Previous studies of CTL responses to influenza peptides in HLA single transgenic mice resulted in the identification of at most one immunodominant epitope. Since HLA-B*3501 is known to present multiple HIV-1-specific T cell epitopes we tested the cellular immune response of HLA-B*3501 transgenic mice to synthetic HTLV-1 peptides mixed with the lipohexapeptideN-palmitoyl-S-[2,3-bis(palmitoyloxy)propyl]cysteinyl-seryl-lysyl-lysyl-lysyl-lysine, which is a biocompatible, Th-epitope-independent adjuvant. Eleven of 37 tested HLA-B*3501 binding peptides mounted a CTL response after threein vitrostimulations. The HLA-B*3501 affinity of peptides correlated with their ability to induce CTL in HLA-B*3501 transgenic mice. Seven peptides derived from env-gp46 (VPSPSSTPLL, VPSSSSTPL, YPSLALAPH, and YPSLALAPA), pol (QAFPQCTIL), gag-p19 (YPGRVNEIL), and tax (GAFLTNVPY) proteins induced peptide-specific CTL. Bulk CTL generated by four peptides derived from env-gp46 (SPPSTPLLY, VPSPSSTPLLY, and VPSPSSTPLL) and pol (QAFPQCTILQY) killed peptide-pulsed and recombinant vaccinia-infected target cells. The latter peptides therefore present T-cell epitopes and are vaccine candidates for our transgenic mouse model.</div></front></TEI><affiliations><list><country><li>Allemagne</li><li>Japon</li><li>Royaume-Uni</li></country><region><li>Région de Kantō</li></region><settlement><li>Tokyo</li></settlement><orgName><li>Université de Tokyo</li></orgName></list><tree><country name="Japon"><region name="Région de Kantō"><name sortKey="Schonbach, Christian" sort="Schonbach, Christian" uniqKey="Schonbach C" first="Christian" last="Schönbach">Christian Schönbach</name></region><name sortKey="Egawa, Kohji" sort="Egawa, Kohji" uniqKey="Egawa K" first="Kohji" last="Egawa">Kohji Egawa</name><name sortKey="Karaki, Sachiko" sort="Karaki, Sachiko" uniqKey="Karaki S" first="Sachiko" last="Karaki">Sachiko Karaki</name><name sortKey="Kariyone, Ai" sort="Kariyone, Ai" uniqKey="Kariyone A" first="Ai" last="Kariyone">Ai Kariyone</name><name sortKey="Nokihara, Kiyoshi" sort="Nokihara, Kiyoshi" uniqKey="Nokihara K" first="Kiyoshi" last="Nokihara">Kiyoshi Nokihara</name><name sortKey="Shida, Hisatoshi" sort="Shida, Hisatoshi" uniqKey="Shida H" first="Hisatoshi" last="Shida">Hisatoshi Shida</name><name sortKey="Takatsu, Kiyoshi" sort="Takatsu, Kiyoshi" uniqKey="Takatsu K" first="Kiyoshi" last="Takatsu">Kiyoshi Takatsu</name><name sortKey="Takiguchi, Masafumi" sort="Takiguchi, Masafumi" uniqKey="Takiguchi M" first="Masafumi" last="Takiguchi">Masafumi Takiguchi</name></country><country name="Royaume-Uni"><noRegion><name sortKey="Bangham, Charles R M" sort="Bangham, Charles R M" uniqKey="Bangham C" first="Charles R. M." last="Bangham">Charles R. M. Bangham</name></noRegion></country><country name="Allemagne"><noRegion><name sortKey="Wiesmuller, Karl Heinz" sort="Wiesmuller, Karl Heinz" uniqKey="Wiesmuller K" first="Karl-Heinz" last="Wiesmüller">Karl-Heinz Wiesmüller</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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