The Clonotypic T Cell Receptor Is a Source of Tumor‐associated Antigens in Cutaneous T Cell Lymphoma
Identifieur interne : 001B52 ( Istex/Corpus ); précédent : 001B51; suivant : 001B53The Clonotypic T Cell Receptor Is a Source of Tumor‐associated Antigens in Cutaneous T Cell Lymphoma
Auteurs : Carole L. Berger ; Jack Longley ; Douglas Hanlon ; Michael Girardi ; Richard EdelsonSource :
- Annals of the New York Academy of Sciences [ 0077-8923 ] ; 2001-09.
Abstract
Abstract: To develop cancer vaccines for the treatment of cutaneous T cell lymphoma (CTCL), immunogenic peptides were identified by two approaches. First, through the use of “reverse immunology” the peptide sequence of the idiotypic region of the β chain of the T cell receptor (TCR) was determined and a series of overlapping peptides synthesized and tested for CD8 T cell recognition. In two patients, the idiotypic CDR3 region provided immunogenic epitopes that were recognized in a class I‐restricted fashion by autologous CD8 T cell lines. In a second strategy, peptides were isolated directly from class I MHC molecules on the CTCL surface and sequenced. A peptide with partial homology to sequences contained in the conserved variable portion of the clonotypic TCR β chain was recognized as immunogenic by autologous CD8 T cells. Therefore, both approaches demonstrated that the clonotypic TCR in CTCL is a source of immunogenic tumor epitopes. To confirm that recognition of TCR‐derived sequences provides immunoprotection against tumor growth, a murine model of T cell lymphoma was studied. The immunogenicity of a thymoma, which lacks cell surface TCR expression, was enhanced by transfection of the β chain of the TCR. The studies reviewed in this paper demonstrate that the TCR can serve as one source for immunogenic tumor peptides in T cell lymphoma in vitro and in vivo. Presentation of TCR epitopes on dendritic cells that express high levels of MHC, costimulatory, and adhesion molecules may provide an effective means for immunization against T cell malignancy.
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DOI: 10.1111/j.1749-6632.2001.tb03715.x
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The immunogenicity of a thymoma, which lacks cell surface TCR expression, was enhanced by transfection of the β chain of the TCR. The studies reviewed in this paper demonstrate that the TCR can serve as one source for immunogenic tumor peptides in T cell lymphoma in vitro and in vivo. 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First, through the use of “reverse immunology” the peptide sequence of the idiotypic region of the β chain of the T cell receptor (TCR) was determined and a series of overlapping peptides synthesized and tested for CD8 T cell recognition. In two patients, the idiotypic CDR3 region provided immunogenic epitopes that were recognized in a class I‐restricted fashion by autologous CD8 T cell lines. In a second strategy, peptides were isolated directly from class I MHC molecules on the CTCL surface and sequenced. A peptide with partial homology to sequences contained in the conserved variable portion of the clonotypic TCR β chain was recognized as immunogenic by autologous CD8 T cells. Therefore, both approaches demonstrated that the clonotypic TCR in CTCL is a source of immunogenic tumor epitopes. To confirm that recognition of TCR‐derived sequences provides immunoprotection against tumor growth, a murine model of T cell lymphoma was studied. The immunogenicity of a thymoma, which lacks cell surface TCR expression, was enhanced by transfection of the β chain of the TCR. The studies reviewed in this paper demonstrate that the TCR can serve as one source for immunogenic tumor peptides in T cell lymphoma in vitro and in vivo. 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A peptide with partial homology to sequences contained in the conserved variable portion of the clonotypic TCR β chain was recognized as immunogenic by autologous CD8 T cells. Therefore, both approaches demonstrated that the clonotypic TCR in CTCL is a source of immunogenic tumor epitopes. To confirm that recognition of TCR‐derived sequences provides immunoprotection against tumor growth, a murine model of T cell lymphoma was studied. The immunogenicity of a thymoma, which lacks cell surface TCR expression, was enhanced by transfection of the β chain of the TCR. The studies reviewed in this paper demonstrate that the TCR can serve as one source for immunogenic tumor peptides in T cell lymphoma <hi rend="italic">in vitro</hi> and <hi rend="italic">in vivo</hi>. Presentation of TCR epitopes on dendritic cells that express high levels of MHC, costimulatory, and adhesion molecules may provide an effective means for immunization against T cell malignancy.</p></abstract><textClass><keywords xml:lang="en"><term xml:id="k1">T cell receptor</term><term xml:id="k2">CD8 T cell recognition</term><term xml:id="k3">“reverse immunology”</term></keywords><keywords rend="tocHeading1"><term>Cutaneous T Cell Lymphoma: Basic and Clinically Relevant Biology: Part III. Designer Immunotherapy</term></keywords></textClass><langUsage><language ident="en"></language></langUsage></profileDesc><revisionDesc><change when="2019-12-20" who="#istex" xml:id="pub2tei">formatting</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-CWWW2JZD-R/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Blackwell Publishing Ltd</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1749-6632</doi><issn type="print">0077-8923</issn><issn type="electronic">1749-6632</issn><idGroup><id type="product" value="NYAS"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="ANNALS OF NEW YORK ACADEMY SCIENCES">Annals of the New York Academy of Sciences</title></titleGroup></publicationMeta><publicationMeta level="part" position="09001"><doi origin="wiley">10.1111/nyas.2001.941.issue-1</doi><titleGroup><title type="main">CUTANEOUS T CELL LYMPHOMA: BASIC AND CLINICALLY RELEVANT BIOLOGY</title></titleGroup><numberingGroup><numbering type="journalVolume" number="941">941</numbering><numbering type="journalIssue">1</numbering></numberingGroup><coverDate startDate="2001-09">September 2001</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="12" status="forIssue"><doi origin="wiley">10.1111/j.1749-6632.2001.tb03715.x</doi><idGroup><id type="unit" value="NYAS106"></id></idGroup><countGroup><count type="pageTotal" number="17"></count></countGroup><titleGroup><title type="tocHeading1">Cutaneous T Cell Lymphoma: Basic and Clinically Relevant Biology: Part III. Designer Immunotherapy</title></titleGroup><eventGroup><event type="firstOnline" date="2006-01-25"></event><event type="publishedOnlineFinalForm" date="2006-01-25"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.5 mode:FullText source:FullText result:FullText" date="2010-04-06"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:4.0.1" date="2014-03-19"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-14"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="106">106</numbering><numbering type="pageLast" number="122">122</numbering></numberingGroup><correspondenceTo>Address for correspondence: Dr. Carole L. Berger, Department of Dermatology, Yale University, School of Medicine, 333 Cedar St., New Haven, CT 06520. Voice: 203‐737‐4024; fax: 203‐785‐7234; <email>Carole.Berger@Yale.edu</email>.</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:NYAS.NYAS106.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="4"></count><count type="tableTotal" number="4"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="19"></count><count type="linksCrossRef" number="41"></count></countGroup><titleGroup><title type="main">The Clonotypic T Cell Receptor Is a Source of Tumor‐associated Antigens in Cutaneous T Cell Lymphoma</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1" corresponding="yes"><personName><givenNames>CAROLE L.</givenNames><familyName>BERGER</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a2"><personName><givenNames>JACK</givenNames><familyName>LONGLEY</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1"><personName><givenNames>DOUGLAS</givenNames><familyName>HANLON</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a1"><personName><givenNames>MICHAEL</givenNames><familyName>GIRARDI</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a1"><personName><givenNames>RICHARD</givenNames><familyName>EDELSON</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="US"><unparsedAffiliation>Department of Dermatology, Yale University, School of Medicine, New Haven, Connecticut 06520, USA</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="US"><unparsedAffiliation>Department of Dermatology, Columbia University, College of Physicians & Surgeons, New York, New York 10032, USA</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">T cell receptor</keyword><keyword xml:id="k2">CD8 T cell recognition</keyword><keyword xml:id="k3">“reverse immunology”</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p><b>A<sc>bstract</sc>: </b> To develop cancer vaccines for the treatment of cutaneous T cell lymphoma (CTCL), immunogenic peptides were identified by two approaches. First, through the use of “reverse immunology” the peptide sequence of the idiotypic region of the β chain of the T cell receptor (TCR) was determined and a series of overlapping peptides synthesized and tested for CD8 T cell recognition. In two patients, the idiotypic CDR3 region provided immunogenic epitopes that were recognized in a class I‐restricted fashion by autologous CD8 T cell lines. In a second strategy, peptides were isolated directly from class I MHC molecules on the CTCL surface and sequenced. A peptide with partial homology to sequences contained in the conserved variable portion of the clonotypic TCR β chain was recognized as immunogenic by autologous CD8 T cells. Therefore, both approaches demonstrated that the clonotypic TCR in CTCL is a source of immunogenic tumor epitopes. To confirm that recognition of TCR‐derived sequences provides immunoprotection against tumor growth, a murine model of T cell lymphoma was studied. The immunogenicity of a thymoma, which lacks cell surface TCR expression, was enhanced by transfection of the β chain of the TCR. The studies reviewed in this paper demonstrate that the TCR can serve as one source for immunogenic tumor peptides in T cell lymphoma <i>in vitro</i> and <i>in vivo</i>. Presentation of TCR epitopes on dendritic cells that express high levels of MHC, costimulatory, and adhesion molecules may provide an effective means for immunization against T cell malignancy.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>The Clonotypic T Cell Receptor Is a Source of Tumor‐associated Antigens in Cutaneous T Cell Lymphoma</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>The Clonotypic T Cell Receptor Is a Source of Tumor‐associated Antigens in Cutaneous T Cell Lymphoma</title></titleInfo><name type="personal"><namePart type="given">CAROLE L.</namePart><namePart type="family">BERGER</namePart><affiliation>Department of Dermatology, Yale University, School of Medicine, New Haven, Connecticut 06520, USA</affiliation><affiliation>E-mail: Carole.Berger@Yale.edu</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">JACK</namePart><namePart type="family">LONGLEY</namePart><affiliation>Department of Dermatology, Columbia University, College of Physicians & Surgeons, New York, New York 10032, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">DOUGLAS</namePart><namePart type="family">HANLON</namePart><affiliation>Department of Dermatology, Yale University, School of Medicine, New Haven, Connecticut 06520, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">MICHAEL</namePart><namePart type="family">GIRARDI</namePart><affiliation>Department of Dermatology, Yale University, School of Medicine, New Haven, Connecticut 06520, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">RICHARD</namePart><namePart type="family">EDELSON</namePart><affiliation>Department of Dermatology, Yale University, School of Medicine, New Haven, Connecticut 06520, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2001-09</dateIssued><copyrightDate encoding="w3cdtf">2001</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><extent unit="figures">4</extent><extent unit="tables">4</extent><extent unit="formulas">0</extent><extent unit="references">19</extent><extent unit="linksCrossRef">41</extent></physicalDescription><abstract lang="en">Abstract: To develop cancer vaccines for the treatment of cutaneous T cell lymphoma (CTCL), immunogenic peptides were identified by two approaches. First, through the use of “reverse immunology” the peptide sequence of the idiotypic region of the β chain of the T cell receptor (TCR) was determined and a series of overlapping peptides synthesized and tested for CD8 T cell recognition. In two patients, the idiotypic CDR3 region provided immunogenic epitopes that were recognized in a class I‐restricted fashion by autologous CD8 T cell lines. In a second strategy, peptides were isolated directly from class I MHC molecules on the CTCL surface and sequenced. A peptide with partial homology to sequences contained in the conserved variable portion of the clonotypic TCR β chain was recognized as immunogenic by autologous CD8 T cells. Therefore, both approaches demonstrated that the clonotypic TCR in CTCL is a source of immunogenic tumor epitopes. To confirm that recognition of TCR‐derived sequences provides immunoprotection against tumor growth, a murine model of T cell lymphoma was studied. The immunogenicity of a thymoma, which lacks cell surface TCR expression, was enhanced by transfection of the β chain of the TCR. The studies reviewed in this paper demonstrate that the TCR can serve as one source for immunogenic tumor peptides in T cell lymphoma in vitro and in vivo. Presentation of TCR epitopes on dendritic cells that express high levels of MHC, costimulatory, and adhesion molecules may provide an effective means for immunization against T cell malignancy.</abstract><subject lang="en"><genre>keywords</genre><topic>T cell receptor</topic><topic>CD8 T cell recognition</topic><topic>“reverse immunology”</topic></subject><relatedItem type="host"><titleInfo><title>Annals of the New York Academy of Sciences</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><identifier type="ISSN">0077-8923</identifier><identifier type="eISSN">1749-6632</identifier><identifier type="DOI">10.1111/(ISSN)1749-6632</identifier><identifier type="PublisherID">NYAS</identifier><part><date>2001</date><detail type="title"><title>CUTANEOUS T CELL LYMPHOMA: BASIC AND CLINICALLY RELEVANT BIOLOGY</title></detail><detail type="volume"><caption>vol.</caption><number>941</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>106</start><end>122</end><total>17</total></extent></part></relatedItem><relatedItem type="references" displayLabel="cit1"><titleInfo><title>Antigenic cancer cells grow progressively in immune hosts without evidence for T cell exhaustion or systemic anergy</title></titleInfo><name type="personal"><namePart type="given">M.</namePart><namePart type="family">Wick</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Wick, M. et al. 1997. 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