Role of a Subdominant H-2Kd-Restricted SV40 Tumor Antigen Cytotoxic T Lymphocyte Epitope in Tumor Rejection
Identifieur interne : 002622 ( Istex/Corpus ); précédent : 002621; suivant : 002623Role of a Subdominant H-2Kd-Restricted SV40 Tumor Antigen Cytotoxic T Lymphocyte Epitope in Tumor Rejection
Auteurs : Romnie S. Newmaster ; Lawrence M. Mylin ; Tong-Ming Fu ; Satvir S. TevethiaSource :
- Virology [ 0042-6822 ] ; 1998.
English descriptors
- KwdEn :
- Teeft :
- Antigen, Antigen presentation, Assay, Bennink, Cancer inst, Cell line, Cell lines, Clone, Culture supplement, Cytotoxic, Cytotoxicity, Cytotoxicity assay, Cytotoxicity assays, Determinant, Dyldgsvkv, Effector, Efficient lysis, Eisenlohr, Encoding, Epitope, Histocompatibility, Immune response, Immunization, Immunocompetent mice, Immunol, Intrascapular region, K5rsv cells, Khtgsv, Khtgsv cells, Knowles, Lymphocyte, Lymphocyte clones, Lyse, Lyse cells, Lysed, Lysis, Major histocompatibility, Mksa, Mksa cells, Mksa stimulator cells, Mksa tumor cells, Mksa tumor challenge, Monoclonal antibodies, Mouse, Mylin, Natl, Newmaster, Nonimmunodominant epitopes, Partial protection, Peptide, Plasmid, Recombinant, Recombinant vaccinia virus, Recombinant vaccinia viruses, Release assay, Restimulated, Schirmbeck, Sequences encoding, Simian, Simian virus, Similar results, Specific lysis, Splenic lymphocytes, Splenocytes, Subdominant, Subdominant epitope, Subdominant epitopes, Synthetic peptide, Synthetic peptides, Tanaka, Target cells, Tevethia, Transgenic mice, Transplantation, Transplantation antigen, Transplantation immunity, Tumor antigen, Tumor cells, Tumor induction, Tumor rejection, Vaccinia, Vaccinia recombinants, Viral, Virol, Virology, Yewdell, Zarling.
Abstract
Abstract: SV40-transformed mKSA cells (H-2d) readily induce progressively growing tumors in adult syngeneic BALB/c mice while expressing the full complement ofH-2dMHC class I antigens. BALB/c mice previously immunized with SV40, soluble SV40 T antigen, or irradiated SV40-transformed syngeneic, allogeneic, or xenogeneic cells reject an mKSA tumor challenge even though these mice have been considered low- or nonresponders to T antigen due to difficulty in demonstrating SV40 T antigen-specific CTL. We have investigated the role of H-2d-restricted CTL in the rejection of SV40 tumors in BALB/c mice. Immunization of BALB/c mice with SV40 induced T antigen-specific CTL which were largely H-2Ld-restricted. However, following repeatedin vitrorestimulation with mKSA cells, CTL emerged which recognized a subdominant H-2Kd-restricted epitope corresponding to T antigen residues 499–507. Immunization of BALB/c mice with a recombinant vaccinia virus expressing the T499–507epitope provided partial protection against a challenge of syngeneic mKSA tumor cells and induced the generation of T499–507-specific CTL. These results indicate that a subdominant H-2Kd-restricted CTL epitope can participate in the rejection of SV40 tumors in BALB/c mice.
Url:
DOI: 10.1006/viro.1998.9148
Links to Exploration step
ISTEX:CB0FE3044540BBD5EADADEEF17B5B1E8D30566CALe document en format XML
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Box 850, Hershey, Pennsylvania, 17033</mods:affiliation></affiliation></author><author><name sortKey="Fu, Tong Ming" sort="Fu, Tong Ming" uniqKey="Fu T" first="Tong-Ming" last="Fu">Tong-Ming Fu</name><affiliation><mods:affiliation>Department of Microbiology and Immunology H107, The Pennsylvania State University College of Medicine, 500 University Drive, P.O. Box 850, Hershey, Pennsylvania, 17033</mods:affiliation></affiliation></author><author><name sortKey="Tevethia, Satvir S" sort="Tevethia, Satvir S" uniqKey="Tevethia S" first="Satvir S." last="Tevethia">Satvir S. Tevethia</name><affiliation><mods:affiliation>Department of Microbiology and Immunology H107, The Pennsylvania State University College of Medicine, 500 University Drive, P.O. 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Newmaster</name><affiliation><mods:affiliation>Department of Microbiology and Immunology H107, The Pennsylvania State University College of Medicine, 500 University Drive, P.O. Box 850, Hershey, Pennsylvania, 17033</mods:affiliation></affiliation></author><author><name sortKey="Mylin, Lawrence M" sort="Mylin, Lawrence M" uniqKey="Mylin L" first="Lawrence M." last="Mylin">Lawrence M. Mylin</name><affiliation><mods:affiliation>Department of Microbiology and Immunology H107, The Pennsylvania State University College of Medicine, 500 University Drive, P.O. Box 850, Hershey, Pennsylvania, 17033</mods:affiliation></affiliation></author><author><name sortKey="Fu, Tong Ming" sort="Fu, Tong Ming" uniqKey="Fu T" first="Tong-Ming" last="Fu">Tong-Ming Fu</name><affiliation><mods:affiliation>Department of Microbiology and Immunology H107, The Pennsylvania State University College of Medicine, 500 University Drive, P.O. Box 850, Hershey, Pennsylvania, 17033</mods:affiliation></affiliation></author><author><name sortKey="Tevethia, Satvir S" sort="Tevethia, Satvir S" uniqKey="Tevethia S" first="Satvir S." last="Tevethia">Satvir S. Tevethia</name><affiliation><mods:affiliation>Department of Microbiology and Immunology H107, The Pennsylvania State University College of Medicine, 500 University Drive, P.O. Box 850, Hershey, Pennsylvania, 17033</mods:affiliation></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="1998">1998</date><biblScope unit="volume">244</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="427">427</biblScope><biblScope unit="page" to="441">441</biblScope></imprint><idno type="ISSN">0042-6822</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0042-6822</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>CTL</term><term>SV40 tumor antigen</term><term>antigen presentation</term><term>subdominant CTL epitope</term><term>tumor immunity</term></keywords><keywords scheme="Teeft" xml:lang="en"><term>Antigen</term><term>Antigen presentation</term><term>Assay</term><term>Bennink</term><term>Cancer inst</term><term>Cell line</term><term>Cell lines</term><term>Clone</term><term>Culture supplement</term><term>Cytotoxic</term><term>Cytotoxicity</term><term>Cytotoxicity assay</term><term>Cytotoxicity assays</term><term>Determinant</term><term>Dyldgsvkv</term><term>Effector</term><term>Efficient lysis</term><term>Eisenlohr</term><term>Encoding</term><term>Epitope</term><term>Histocompatibility</term><term>Immune response</term><term>Immunization</term><term>Immunocompetent mice</term><term>Immunol</term><term>Intrascapular region</term><term>K5rsv cells</term><term>Khtgsv</term><term>Khtgsv cells</term><term>Knowles</term><term>Lymphocyte</term><term>Lymphocyte clones</term><term>Lyse</term><term>Lyse cells</term><term>Lysed</term><term>Lysis</term><term>Major histocompatibility</term><term>Mksa</term><term>Mksa cells</term><term>Mksa stimulator cells</term><term>Mksa tumor cells</term><term>Mksa tumor challenge</term><term>Monoclonal antibodies</term><term>Mouse</term><term>Mylin</term><term>Natl</term><term>Newmaster</term><term>Nonimmunodominant epitopes</term><term>Partial protection</term><term>Peptide</term><term>Plasmid</term><term>Recombinant</term><term>Recombinant vaccinia virus</term><term>Recombinant vaccinia viruses</term><term>Release assay</term><term>Restimulated</term><term>Schirmbeck</term><term>Sequences encoding</term><term>Simian</term><term>Simian virus</term><term>Similar results</term><term>Specific lysis</term><term>Splenic lymphocytes</term><term>Splenocytes</term><term>Subdominant</term><term>Subdominant epitope</term><term>Subdominant epitopes</term><term>Synthetic peptide</term><term>Synthetic peptides</term><term>Tanaka</term><term>Target cells</term><term>Tevethia</term><term>Transgenic mice</term><term>Transplantation</term><term>Transplantation antigen</term><term>Transplantation immunity</term><term>Tumor antigen</term><term>Tumor cells</term><term>Tumor induction</term><term>Tumor rejection</term><term>Vaccinia</term><term>Vaccinia recombinants</term><term>Viral</term><term>Virol</term><term>Virology</term><term>Yewdell</term><term>Zarling</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: SV40-transformed mKSA cells (H-2d) readily induce progressively growing tumors in adult syngeneic BALB/c mice while expressing the full complement ofH-2dMHC class I antigens. BALB/c mice previously immunized with SV40, soluble SV40 T antigen, or irradiated SV40-transformed syngeneic, allogeneic, or xenogeneic cells reject an mKSA tumor challenge even though these mice have been considered low- or nonresponders to T antigen due to difficulty in demonstrating SV40 T antigen-specific CTL. We have investigated the role of H-2d-restricted CTL in the rejection of SV40 tumors in BALB/c mice. Immunization of BALB/c mice with SV40 induced T antigen-specific CTL which were largely H-2Ld-restricted. However, following repeatedin vitrorestimulation with mKSA cells, CTL emerged which recognized a subdominant H-2Kd-restricted epitope corresponding to T antigen residues 499–507. Immunization of BALB/c mice with a recombinant vaccinia virus expressing the T499–507epitope provided partial protection against a challenge of syngeneic mKSA tumor cells and induced the generation of T499–507-specific CTL. 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Newmaster</name><affiliations><json:string>Department of Microbiology and Immunology H107, The Pennsylvania State University College of Medicine, 500 University Drive, P.O. Box 850, Hershey, Pennsylvania, 17033</json:string></affiliations></json:item><json:item><name>Lawrence M. Mylin</name><affiliations><json:string>Department of Microbiology and Immunology H107, The Pennsylvania State University College of Medicine, 500 University Drive, P.O. Box 850, Hershey, Pennsylvania, 17033</json:string></affiliations></json:item><json:item><name>Tong-Ming Fu</name><affiliations><json:string>Department of Microbiology and Immunology H107, The Pennsylvania State University College of Medicine, 500 University Drive, P.O. Box 850, Hershey, Pennsylvania, 17033</json:string></affiliations></json:item><json:item><name>Satvir S. Tevethia</name><affiliations><json:string>Department of Microbiology and Immunology H107, The Pennsylvania State University College of Medicine, 500 University Drive, P.O. Box 850, Hershey, Pennsylvania, 17033</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>tumor immunity</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>antigen presentation</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>CTL</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>SV40 tumor antigen</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>subdominant CTL epitope</value></json:item></subject><arkIstex>ark:/67375/6H6-G3PBDD6P-X</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>Full-length article</json:string></originalGenre><abstract>Abstract: SV40-transformed mKSA cells (H-2d) readily induce progressively growing tumors in adult syngeneic BALB/c mice while expressing the full complement ofH-2dMHC class I antigens. BALB/c mice previously immunized with SV40, soluble SV40 T antigen, or irradiated SV40-transformed syngeneic, allogeneic, or xenogeneic cells reject an mKSA tumor challenge even though these mice have been considered low- or nonresponders to T antigen due to difficulty in demonstrating SV40 T antigen-specific CTL. We have investigated the role of H-2d-restricted CTL in the rejection of SV40 tumors in BALB/c mice. Immunization of BALB/c mice with SV40 induced T antigen-specific CTL which were largely H-2Ld-restricted. However, following repeatedin vitrorestimulation with mKSA cells, CTL emerged which recognized a subdominant H-2Kd-restricted epitope corresponding to T antigen residues 499–507. Immunization of BALB/c mice with a recombinant vaccinia virus expressing the T499–507epitope provided partial protection against a challenge of syngeneic mKSA tumor cells and induced the generation of T499–507-specific CTL. These results indicate that a subdominant H-2Kd-restricted CTL epitope can participate in the rejection of SV40 tumors in BALB/c mice.</abstract><qualityIndicators><score>9.052</score><pdfWordCount>9197</pdfWordCount><pdfCharCount>58795</pdfCharCount><pdfVersion>1.2</pdfVersion><pdfPageCount>15</pdfPageCount><pdfPageSize>532 x 717 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractWordCount>171</abstractWordCount><abstractCharCount>1245</abstractCharCount><keywordCount>5</keywordCount></qualityIndicators><title>Role of a Subdominant H-2Kd-Restricted SV40 Tumor Antigen Cytotoxic T Lymphocyte Epitope in Tumor Rejection</title><pmid><json:string>9601511</json:string></pmid><pii><json:string>S0042-6822(98)99148-6</json:string></pii><genre><json:string>research-article</json:string></genre><host><title>Virology</title><language><json:string>unknown</json:string></language><publicationDate>1998</publicationDate><issn><json:string>0042-6822</json:string></issn><pii><json:string>S0042-6822(00)X0092-X</json:string></pii><volume>244</volume><issue>2</issue><pages><first>427</first><last>441</last></pages><genre><json:string>journal</json:string></genre></host><namedEntities><unitex><date><json:string>1998</json:string></date><geogName></geogName><orgName><json:string>Jackson Laboratories</json:string><json:string>National Cancer Institute, National Institutes of Health, Bethesda, MD</json:string><json:string>Merck Research Laboratories, Dept</json:string><json:string>Sigma Chemical Co.</json:string><json:string>The Pennsylvania State University</json:string></orgName><orgName_funder></orgName_funder><orgName_provider></orgName_provider><persName><json:string>P.O. Box</json:string><json:string>S. Tevethia</json:string><json:string>Schirmbeck</json:string><json:string>Tong-Ming Fu</json:string><json:string>Lawrence M. Mylin</json:string><json:string>In</json:string><json:string>Facility</json:string><json:string>Carol Reiss</json:string><json:string>Tag</json:string><json:string>Melanie Epler</json:string><json:string>Jonathan Yewdell</json:string><json:string>Jack Bennink</json:string><json:string>Barbara Knowles</json:string></persName><placeName><json:string>Bedford</json:string><json:string>Cytotoxicity</json:string><json:string>San Diego</json:string><json:string>ME</json:string><json:string>CA</json:string><json:string>MA</json:string><json:string>Cambridge</json:string><json:string>Bar Harbor</json:string></placeName><ref_url></ref_url><ref_bibl><json:string>Oukka et al., 1996</json:string><json:string>Tevethia, 1990</json:string><json:string>Chen et al., 1994</json:string><json:string>Hanahan, 1985</json:string><json:string>Shearer et al., 1993</json:string><json:string>Deng et al., 1997</json:string><json:string>Flyer et al., 1983</json:string><json:string>Tevethia et al., 1974a</json:string><json:string>Schirmbeck et al., 1996</json:string><json:string>Tevethia et al., 1980</json:string><json:string>Mylin et al., 1995a</json:string><json:string>Lippolis et al., 1995</json:string><json:string>Ornitz et al., 1987</json:string><json:string>Levine, 1989</json:string><json:string>Deckhut et al., 1992</json:string><json:string>Jennings et al., 1985</json:string><json:string>Eisenlohr et al., 1992</json:string><json:string>Tevethia and McMillan, 1974</json:string><json:string>reviewed in Tevethia, 1980</json:string><json:string>Tevethia et al., 1979</json:string><json:string>Pfizenmaier et al., 1978</json:string><json:string>Yellen-Shaw et al., 1997</json:string><json:string>Restifo et al., 1993</json:string><json:string>Flyer et al., 1982</json:string><json:string>Kit et al., 1969</json:string><json:string>Oldstone et al., 1995</json:string><json:string>Marguiles et al., 1983</json:string><json:string>Niedermann et al., 1995</json:string><json:string>Bright et al., 1996</json:string><json:string>Fu et al., 1998</json:string><json:string>Fu et al.</json:string><json:string>Lill et al., 1992</json:string><json:string>Sparer et al., 1997</json:string><json:string>Tanaka et al., 1989</json:string><json:string>Kagi et al., 1996</json:string><json:string>reviewed in Tevethia, 1990</json:string><json:string>Yewdell et al., 1993</json:string><json:string>Vitiello et al., 1996</json:string><json:string>Gooding, 1979</json:string><json:string>Brinster et al., 1984</json:string><json:string>Zarling and Tevethia, 1973a</json:string><json:string>data not shown; Zarling and Tevethia, 1973a</json:string><json:string>Schirmbeck et al. 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(1978)</json:string><json:string>Gooding, 1982</json:string><json:string>reviewed in Tevethia, 1980, 1990</json:string><json:string>Kalderon and Smith, 1984</json:string><json:string>Feltkamp et al., 1995</json:string><json:string>Deckhut and Tevethia, 1992</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/6H6-G3PBDD6P-X</json:string></ark><categories><wos><json:string>1 - science</json:string><json:string>2 - virology</json:string></wos><scienceMetrix><json:string>1 - health sciences</json:string><json:string>2 - biomedical research</json:string><json:string>3 - virology</json:string></scienceMetrix><scopus><json:string>1 - Life Sciences</json:string><json:string>2 - Immunology and Microbiology</json:string><json:string>3 - Virology</json:string></scopus><inist><json:string>1 - sciences appliquees, technologies et medecines</json:string><json:string>2 - sciences biologiques et medicales</json:string><json:string>3 - sciences medicales</json:string><json:string>4 - immunopathologie</json:string></inist></categories><publicationDate>1998</publicationDate><copyrightDate>1998</copyrightDate><doi><json:string>10.1006/viro.1998.9148</json:string></doi><id>CB0FE3044540BBD5EADADEEF17B5B1E8D30566CA</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-G3PBDD6P-X/fulltext.pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-G3PBDD6P-X/bundle.zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/ark:/67375/6H6-G3PBDD6P-X/fulltext.tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Role of a Subdominant H-2Kd-Restricted SV40 Tumor Antigen Cytotoxic T Lymphocyte Epitope in Tumor Rejection</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher scheme="https://scientific-publisher.data.istex.fr">ELSEVIER</publisher><availability><licence><p>©1998 Academic Press</p></licence><p scheme="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M">elsevier</p></availability><date>1998</date></publicationStmt><notesStmt><note type="research-article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</note><note type="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note><note type="content">Section title: Regular Article</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Role of a Subdominant H-2Kd-Restricted SV40 Tumor Antigen Cytotoxic T Lymphocyte Epitope in Tumor Rejection</title><author xml:id="author-0000"><persName><forename type="first">Romnie S.</forename><surname>Newmaster</surname></persName><affiliation>Department of Microbiology and Immunology H107, The Pennsylvania State University College of Medicine, 500 University Drive, P.O. Box 850, Hershey, Pennsylvania, 17033</affiliation></author><author xml:id="author-0001"><persName><forename type="first">Lawrence M.</forename><surname>Mylin</surname></persName><affiliation>Department of Microbiology and Immunology H107, The Pennsylvania State University College of Medicine, 500 University Drive, P.O. Box 850, Hershey, Pennsylvania, 17033</affiliation></author><author xml:id="author-0002"><persName><forename type="first">Tong-Ming</forename><surname>Fu</surname></persName><note type="biography">Present address: Merck Research Laboratories, Dept. of Virus and Cell Biology, West Point, PA 19486.</note><affiliation>Present address: Merck Research Laboratories, Dept. of Virus and Cell Biology, West Point, PA 19486.</affiliation><affiliation>Department of Microbiology and Immunology H107, The Pennsylvania State University College of Medicine, 500 University Drive, P.O. Box 850, Hershey, Pennsylvania, 17033</affiliation></author><author xml:id="author-0003"><persName><forename type="first">Satvir S.</forename><surname>Tevethia</surname></persName><affiliation>To whom correspondence and reprint requests should be addressed. E-mail:sst1@psu.edu. Fax: (717) 531-5578.</affiliation><affiliation>Department of Microbiology and Immunology H107, The Pennsylvania State University College of Medicine, 500 University Drive, P.O. Box 850, Hershey, Pennsylvania, 17033</affiliation></author><idno type="istex">CB0FE3044540BBD5EADADEEF17B5B1E8D30566CA</idno><idno type="ark">ark:/67375/6H6-G3PBDD6P-X</idno><idno type="DOI">10.1006/viro.1998.9148</idno><idno type="PII">S0042-6822(98)99148-6</idno></analytic><monogr><title level="j">Virology</title><title level="j" type="abbrev">YVIRO</title><idno type="pISSN">0042-6822</idno><idno type="PII">S0042-6822(00)X0092-X</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1998"></date><biblScope unit="volume">244</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="427">427</biblScope><biblScope unit="page" to="441">441</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1998</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Abstract: SV40-transformed mKSA cells (H-2d) readily induce progressively growing tumors in adult syngeneic BALB/c mice while expressing the full complement ofH-2dMHC class I antigens. BALB/c mice previously immunized with SV40, soluble SV40 T antigen, or irradiated SV40-transformed syngeneic, allogeneic, or xenogeneic cells reject an mKSA tumor challenge even though these mice have been considered low- or nonresponders to T antigen due to difficulty in demonstrating SV40 T antigen-specific CTL. We have investigated the role of H-2d-restricted CTL in the rejection of SV40 tumors in BALB/c mice. Immunization of BALB/c mice with SV40 induced T antigen-specific CTL which were largely H-2Ld-restricted. However, following repeatedin vitrorestimulation with mKSA cells, CTL emerged which recognized a subdominant H-2Kd-restricted epitope corresponding to T antigen residues 499–507. Immunization of BALB/c mice with a recombinant vaccinia virus expressing the T499–507epitope provided partial protection against a challenge of syngeneic mKSA tumor cells and induced the generation of T499–507-specific CTL. These results indicate that a subdominant H-2Kd-restricted CTL epitope can participate in the rejection of SV40 tumors in BALB/c mice.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>tumor immunity</term></item><item><term>antigen presentation</term></item><item><term>CTL</term></item><item><term>SV40 tumor antigen</term></item><item><term>subdominant CTL epitope</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1998-02-13">Modified</change><change when="1998">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-G3PBDD6P-X/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: tail"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla" xml:lang="en"><item-info><jid>YVIRO</jid><aid>99148</aid><ce:pii>S0042-6822(98)99148-6</ce:pii><ce:doi>10.1006/viro.1998.9148</ce:doi><ce:copyright type="full-transfer" year="1998">Academic Press</ce:copyright></item-info><head><ce:dochead><ce:textfn>Regular Article</ce:textfn></ce:dochead><ce:title>Role of a Subdominant H-2K<ce:sup>d</ce:sup>-Restricted SV40 Tumor Antigen Cytotoxic T Lymphocyte Epitope in Tumor Rejection</ce:title><ce:author-group><ce:author><ce:given-name>Romnie S.</ce:given-name><ce:surname>Newmaster</ce:surname></ce:author><ce:author><ce:given-name>Lawrence M.</ce:given-name><ce:surname>Mylin</ce:surname></ce:author><ce:author><ce:given-name>Tong-Ming</ce:given-name><ce:surname>Fu</ce:surname><ce:cross-ref refid="VY989148FN1"><ce:sup>1</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Satvir S.</ce:given-name><ce:surname>Tevethia</ce:surname><ce:cross-ref refid="VY989148FN2"><ce:sup>2</ce:sup></ce:cross-ref></ce:author><ce:affiliation><ce:textfn>Department of Microbiology and Immunology H107, The Pennsylvania State University College of Medicine, 500 University Drive, P.O. Box 850, Hershey, Pennsylvania, 17033</ce:textfn></ce:affiliation><ce:footnote id="VY989148FN1"><ce:label>1</ce:label><ce:note-para>Present address: Merck Research Laboratories, Dept. of Virus and Cell Biology, West Point, PA 19486.</ce:note-para></ce:footnote><ce:footnote id="VY989148FN2"><ce:label>2</ce:label><ce:note-para>To whom correspondence and reprint requests should be addressed. E-mail:sst1@psu.edu. Fax: (717) 531-5578.</ce:note-para></ce:footnote></ce:author-group><ce:date-received day="7" month="1" year="1998"></ce:date-received><ce:date-revised day="13" month="2" year="1998"></ce:date-revised><ce:date-accepted day="13" month="3" year="1998"></ce:date-accepted><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>SV40-transformed mKSA cells (<ce:italic>H-2<ce:sup>d</ce:sup></ce:italic>) readily induce progressively growing tumors in adult syngeneic BALB/c mice while expressing the full complement of<ce:italic>H-2<ce:sup>d</ce:sup></ce:italic>MHC class I antigens. BALB/c mice previously immunized with SV40, soluble SV40 T antigen, or irradiated SV40-transformed syngeneic, allogeneic, or xenogeneic cells reject an mKSA tumor challenge even though these mice have been considered low- or nonresponders to T antigen due to difficulty in demonstrating SV40 T antigen-specific CTL. We have investigated the role of H-2<ce:sup>d</ce:sup>-restricted CTL in the rejection of SV40 tumors in BALB/c mice. Immunization of BALB/c mice with SV40 induced T antigen-specific CTL which were largely H-2L<ce:sup>d</ce:sup>-restricted. However, following repeated<ce:italic>in vitro</ce:italic>restimulation with mKSA cells, CTL emerged which recognized a subdominant H-2K<ce:sup>d</ce:sup>-restricted epitope corresponding to T antigen residues 499–507. Immunization of BALB/c mice with a recombinant vaccinia virus expressing the T<ce:inf>499–507</ce:inf>epitope provided partial protection against a challenge of syngeneic mKSA tumor cells and induced the generation of T<ce:inf>499–507</ce:inf>-specific CTL. These results indicate that a subdominant H-2K<ce:sup>d</ce:sup>-restricted CTL epitope can participate in the rejection of SV40 tumors in BALB/c mice.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>tumor immunity</ce:text></ce:keyword><ce:keyword><ce:text>antigen presentation</ce:text></ce:keyword><ce:keyword><ce:text>CTL</ce:text></ce:keyword><ce:keyword><ce:text>SV40 tumor antigen</ce:text></ce:keyword><ce:keyword><ce:text>subdominant CTL epitope</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Role of a Subdominant H-2Kd-Restricted SV40 Tumor Antigen Cytotoxic T Lymphocyte Epitope in Tumor Rejection</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Role of a Subdominant H-2K</title></titleInfo><name type="personal"><namePart type="given">Romnie S.</namePart><namePart type="family">Newmaster</namePart><affiliation>Department of Microbiology and Immunology H107, The Pennsylvania State University College of Medicine, 500 University Drive, P.O. Box 850, Hershey, Pennsylvania, 17033</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Lawrence M.</namePart><namePart type="family">Mylin</namePart><affiliation>Department of Microbiology and Immunology H107, The Pennsylvania State University College of Medicine, 500 University Drive, P.O. Box 850, Hershey, Pennsylvania, 17033</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Tong-Ming</namePart><namePart type="family">Fu</namePart><affiliation>Department of Microbiology and Immunology H107, The Pennsylvania State University College of Medicine, 500 University Drive, P.O. Box 850, Hershey, Pennsylvania, 17033</affiliation><description>Present address: Merck Research Laboratories, Dept. of Virus and Cell Biology, West Point, PA 19486.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Satvir S.</namePart><namePart type="family">Tevethia</namePart><affiliation>Department of Microbiology and Immunology H107, The Pennsylvania State University College of Medicine, 500 University Drive, P.O. Box 850, Hershey, Pennsylvania, 17033</affiliation><description>To whom correspondence and reprint requests should be addressed. E-mail:sst1@psu.edu. Fax: (717) 531-5578.</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1998</dateIssued><dateModified encoding="w3cdtf">1998-02-13</dateModified><copyrightDate encoding="w3cdtf">1998</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><abstract lang="en">Abstract: SV40-transformed mKSA cells (H-2d) readily induce progressively growing tumors in adult syngeneic BALB/c mice while expressing the full complement ofH-2dMHC class I antigens. BALB/c mice previously immunized with SV40, soluble SV40 T antigen, or irradiated SV40-transformed syngeneic, allogeneic, or xenogeneic cells reject an mKSA tumor challenge even though these mice have been considered low- or nonresponders to T antigen due to difficulty in demonstrating SV40 T antigen-specific CTL. We have investigated the role of H-2d-restricted CTL in the rejection of SV40 tumors in BALB/c mice. Immunization of BALB/c mice with SV40 induced T antigen-specific CTL which were largely H-2Ld-restricted. However, following repeatedin vitrorestimulation with mKSA cells, CTL emerged which recognized a subdominant H-2Kd-restricted epitope corresponding to T antigen residues 499–507. Immunization of BALB/c mice with a recombinant vaccinia virus expressing the T499–507epitope provided partial protection against a challenge of syngeneic mKSA tumor cells and induced the generation of T499–507-specific CTL. These results indicate that a subdominant H-2Kd-restricted CTL epitope can participate in the rejection of SV40 tumors in BALB/c mice.</abstract><note type="content">Section title: Regular Article</note><subject lang="en"><genre>Keywords</genre><topic>tumor immunity</topic><topic>antigen presentation</topic><topic>CTL</topic><topic>SV40 tumor antigen</topic><topic>subdominant CTL epitope</topic></subject><relatedItem type="host"><titleInfo><title>Virology</title></titleInfo><titleInfo type="abbreviated"><title>YVIRO</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1998</dateIssued></originInfo><identifier type="ISSN">0042-6822</identifier><identifier type="PII">S0042-6822(00)X0092-X</identifier><part><date>1998</date><detail type="volume"><number>244</number><caption>vol.</caption></detail><detail type="issue"><number>2</number><caption>no.</caption></detail><extent unit="issue-pages"><start>245</start><end>574</end></extent><extent unit="pages"><start>427</start><end>441</end></extent></part></relatedItem><identifier type="istex">CB0FE3044540BBD5EADADEEF17B5B1E8D30566CA</identifier><identifier type="ark">ark:/67375/6H6-G3PBDD6P-X</identifier><identifier type="DOI">10.1006/viro.1998.9148</identifier><identifier type="PII">S0042-6822(98)99148-6</identifier><accessCondition type="use and reproduction" contentType="copyright">©1998 Academic Press</accessCondition><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M">elsevier</recordContentSource><recordOrigin>Academic Press, ©1998</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-G3PBDD6P-X/record.json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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