Schistosoma mansoni: Genetic Restriction and Cytokine Profile of the CD4 + T Helper Cell Response to Dominant Epitope Peptide of Major Egg Antigen Sm-p40
Identifieur interne : 001E06 ( Istex/Corpus ); précédent : 001E05; suivant : 001E07Schistosoma mansoni: Genetic Restriction and Cytokine Profile of the CD4 + T Helper Cell Response to Dominant Epitope Peptide of Major Egg Antigen Sm-p40
Auteurs : Hector J. Hernandez ; Clark M. Edson ; Donald A. Harn ; Christopher J. Ianelli ; Miguel J. StadeckerSource :
- Experimental Parasitology [ 0014-4894 ] ; 1998.
English descriptors
- KwdEn :
- Teeft :
- Amino, Amino acids, Antigen, Background values, Boros, Cell epitopes, Cell hybridoma responses, Cell hybridomas, Cell proliferative responses, Cell response, Clonal level, Culture supernatants, Cytokine, Cytokine profile, Dominant epitope peptide, Epitope, European journal, Granuloma, Granuloma formation, Hybridoma, Immunology, Lymph, Lymph node cells, Major schistosomal, Mansoni, Mesenteric lymph nodes, Mouse, Mouse strains, Node, Peptide, Polyclonal, Proliferative, Schistosoma, Schistosoma mansoni, Schistosomal, Similar results, Stadecker, Stimulatory, Stimulatory peptides, Triplicate cultures, Tropical diseases, Various mouse strains.
Abstract
Abstract: Hernandez, H. J., Edson, C. M., Harn, D. A., Ianelli, C. J., and Stadecker, M. J. 1998.Schistosoma mansoni: Genetic restriction and cytokine profile of the CD4+ T helper cell response to dominant epitope peptide of major egg antigen Sm-p40.Experimental Parasitology90, 122–130. Granuloma formation in schistosomiasis is mediated by MHC class II-restricted CD4 + T helper lymphocytes sensitized to egg antigens. We previously reported that C3H mice, which develop large granulomas, display strong CD4 + T helper cell responses to the major egg antigen Sm-p40. Moreover, all members of a panel of egg antigen-specific T cell hybridomas responded to the Sm-p40 antigen. Given the significance of the Sm-p40 molecule in the C3H T cell repertoire against schistosomal egg antigens, the current work was undertaken to map its immunogenic epitopes, using a library of 15 synthetic overlapping 30-mer peptides. The dominant epitope recognized by polyclonal CD4 + Th cells was located in peptide 10 (amino acids 229–258); subdominant epitopes were detected in peptides 8 (amino acids 179–208) and 12 (amino acids 279–308). The anti-Sm-p40 T cell hybridomas variously responded to any one of the same three stimulatory peptides. Furthermore, studies with various mouse strains demonstrated that a strong anti-Sm-p40 response was restricted by H-2k. Interestingly, the cells responding to peptide 10 and to the Sm-p40 antigen only secreted IL-2 and IFN-γ, but not IL-4 and IL-10, indicating that they are entirely of the Th-1-type, a subset with demonstrated capacity to mediate egg granuloma formation. The identification of dominant epitopes within key egg antigens offers opportunities for desensitization of the CD4 + Th cells that mediate pathology in schistosomia sis.
Url:
DOI: 10.1006/expr.1998.4309
Links to Exploration step
ISTEX:E6F16FE72E07A87A2C260BEE903363C126A35D13Le document en format XML
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Edson</name><affiliation><mods:affiliation>Department of Pathology, Tufts University School of Medicine, Boston, Massachusetts, 02111, U.S.A.</mods:affiliation></affiliation></author><author><name sortKey="Harn, Donald A" sort="Harn, Donald A" uniqKey="Harn D" first="Donald A." last="Harn">Donald A. Harn</name><affiliation><mods:affiliation>Department of Tropical Public Health, Harvard School of Public Health, Boston, Massachusetts, 02115, U.S.A.</mods:affiliation></affiliation></author><author><name sortKey="Ianelli, Christopher J" sort="Ianelli, Christopher J" uniqKey="Ianelli C" first="Christopher J." last="Ianelli">Christopher J. Ianelli</name><affiliation><mods:affiliation>Department of Pathology, Tufts University School of Medicine, Boston, Massachusetts, 02111, U.S.A.</mods:affiliation></affiliation></author><author><name sortKey="Stadecker, Miguel J" sort="Stadecker, Miguel J" uniqKey="Stadecker M" first="Miguel J." last="Stadecker">Miguel J. 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Hernandez</name><affiliation><mods:affiliation>Department of Pathology, Tufts University School of Medicine, Boston, Massachusetts, 02111, U.S.A.</mods:affiliation></affiliation></author><author><name sortKey="Edson, Clark M" sort="Edson, Clark M" uniqKey="Edson C" first="Clark M." last="Edson">Clark M. Edson</name><affiliation><mods:affiliation>Department of Pathology, Tufts University School of Medicine, Boston, Massachusetts, 02111, U.S.A.</mods:affiliation></affiliation></author><author><name sortKey="Harn, Donald A" sort="Harn, Donald A" uniqKey="Harn D" first="Donald A." last="Harn">Donald A. Harn</name><affiliation><mods:affiliation>Department of Tropical Public Health, Harvard School of Public Health, Boston, Massachusetts, 02115, U.S.A.</mods:affiliation></affiliation></author><author><name sortKey="Ianelli, Christopher J" sort="Ianelli, Christopher J" uniqKey="Ianelli C" first="Christopher J." last="Ianelli">Christopher J. Ianelli</name><affiliation><mods:affiliation>Department of Pathology, Tufts University School of Medicine, Boston, Massachusetts, 02111, U.S.A.</mods:affiliation></affiliation></author><author><name sortKey="Stadecker, Miguel J" sort="Stadecker, Miguel J" uniqKey="Stadecker M" first="Miguel J." last="Stadecker">Miguel J. Stadecker</name><affiliation><mods:affiliation>Department of Pathology, Tufts University School of Medicine, Boston, Massachusetts, 02111, U.S.A.</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Experimental Parasitology</title><title level="j" type="abbrev">YEXPR</title><idno type="ISSN">0014-4894</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1998">1998</date><biblScope unit="volume">90</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="122">122</biblScope><biblScope unit="page" to="130">130</biblScope></imprint><idno type="ISSN">0014-4894</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0014-4894</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>MHC restriction</term><term>SEA, schistosomal egg antigens.</term><term>Schistosoma mansoni</term><term>T cell epitopes</term><term>T cell subsets</term><term>cytokines</term><term>egg antigens</term></keywords><keywords scheme="Teeft" xml:lang="en"><term>Amino</term><term>Amino acids</term><term>Antigen</term><term>Background values</term><term>Boros</term><term>Cell epitopes</term><term>Cell hybridoma responses</term><term>Cell hybridomas</term><term>Cell proliferative responses</term><term>Cell response</term><term>Clonal level</term><term>Culture supernatants</term><term>Cytokine</term><term>Cytokine profile</term><term>Dominant epitope peptide</term><term>Epitope</term><term>European journal</term><term>Granuloma</term><term>Granuloma formation</term><term>Hybridoma</term><term>Immunology</term><term>Lymph</term><term>Lymph node cells</term><term>Major schistosomal</term><term>Mansoni</term><term>Mesenteric lymph nodes</term><term>Mouse</term><term>Mouse strains</term><term>Node</term><term>Peptide</term><term>Polyclonal</term><term>Proliferative</term><term>Schistosoma</term><term>Schistosoma mansoni</term><term>Schistosomal</term><term>Similar results</term><term>Stadecker</term><term>Stimulatory</term><term>Stimulatory peptides</term><term>Triplicate cultures</term><term>Tropical diseases</term><term>Various mouse strains</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Hernandez, H. J., Edson, C. M., Harn, D. A., Ianelli, C. J., and Stadecker, M. J. 1998.Schistosoma mansoni: Genetic restriction and cytokine profile of the CD4+ T helper cell response to dominant epitope peptide of major egg antigen Sm-p40.Experimental Parasitology90, 122–130. Granuloma formation in schistosomiasis is mediated by MHC class II-restricted CD4 + T helper lymphocytes sensitized to egg antigens. We previously reported that C3H mice, which develop large granulomas, display strong CD4 + T helper cell responses to the major egg antigen Sm-p40. Moreover, all members of a panel of egg antigen-specific T cell hybridomas responded to the Sm-p40 antigen. Given the significance of the Sm-p40 molecule in the C3H T cell repertoire against schistosomal egg antigens, the current work was undertaken to map its immunogenic epitopes, using a library of 15 synthetic overlapping 30-mer peptides. The dominant epitope recognized by polyclonal CD4 + Th cells was located in peptide 10 (amino acids 229–258); subdominant epitopes were detected in peptides 8 (amino acids 179–208) and 12 (amino acids 279–308). The anti-Sm-p40 T cell hybridomas variously responded to any one of the same three stimulatory peptides. Furthermore, studies with various mouse strains demonstrated that a strong anti-Sm-p40 response was restricted by H-2k. Interestingly, the cells responding to peptide 10 and to the Sm-p40 antigen only secreted IL-2 and IFN-γ, but not IL-4 and IL-10, indicating that they are entirely of the Th-1-type, a subset with demonstrated capacity to mediate egg granuloma formation. The identification of dominant epitopes within key egg antigens offers opportunities for desensitization of the CD4 + Th cells that mediate pathology in schistosomia sis.</div></front></TEI><istex><corpusName>elsevier</corpusName><keywords><teeft><json:string>epitope</json:string><json:string>peptide</json:string><json:string>hybridoma</json:string><json:string>mansoni</json:string><json:string>immunology</json:string><json:string>schistosoma</json:string><json:string>cytokine</json:string><json:string>schistosoma mansoni</json:string><json:string>node</json:string><json:string>granuloma</json:string><json:string>schistosomal</json:string><json:string>cell hybridomas</json:string><json:string>stadecker</json:string><json:string>boros</json:string><json:string>cell epitopes</json:string><json:string>granuloma formation</json:string><json:string>proliferative</json:string><json:string>amino acids</json:string><json:string>polyclonal</json:string><json:string>european journal</json:string><json:string>stimulatory peptides</json:string><json:string>amino</json:string><json:string>similar results</json:string><json:string>mouse strains</json:string><json:string>dominant epitope peptide</json:string><json:string>cell proliferative responses</json:string><json:string>major schistosomal</json:string><json:string>cell hybridoma responses</json:string><json:string>lymph</json:string><json:string>stimulatory</json:string><json:string>triplicate cultures</json:string><json:string>tropical diseases</json:string><json:string>mesenteric lymph nodes</json:string><json:string>lymph node cells</json:string><json:string>cytokine profile</json:string><json:string>clonal level</json:string><json:string>cell response</json:string><json:string>background values</json:string><json:string>culture supernatants</json:string><json:string>various mouse strains</json:string><json:string>antigen</json:string><json:string>mouse</json:string></teeft></keywords><author><json:item><name>Hector J. Hernandez</name><affiliations><json:string>Department of Pathology, Tufts University School of Medicine, Boston, Massachusetts, 02111, U.S.A.</json:string></affiliations></json:item><json:item><name>Clark M. Edson</name><affiliations><json:string>Department of Pathology, Tufts University School of Medicine, Boston, Massachusetts, 02111, U.S.A.</json:string></affiliations></json:item><json:item><name>Donald A. Harn</name><affiliations><json:string>Department of Tropical Public Health, Harvard School of Public Health, Boston, Massachusetts, 02115, U.S.A.</json:string></affiliations></json:item><json:item><name>Christopher J. Ianelli</name><affiliations><json:string>Department of Pathology, Tufts University School of Medicine, Boston, Massachusetts, 02111, U.S.A.</json:string></affiliations></json:item><json:item><name>Miguel J. Stadecker</name><affiliations><json:string>Department of Pathology, Tufts University School of Medicine, Boston, Massachusetts, 02111, U.S.A.</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Schistosoma mansoni</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>egg antigens</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>T cell epitopes</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>T cell subsets</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>MHC restriction</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>cytokines</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>SEA, schistosomal egg antigens.</value></json:item></subject><arkIstex>ark:/67375/6H6-80ZH2CVW-G</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>Full-length article</json:string></originalGenre><abstract>Abstract: Hernandez, H. J., Edson, C. M., Harn, D. A., Ianelli, C. J., and Stadecker, M. J. 1998.Schistosoma mansoni: Genetic restriction and cytokine profile of the CD4+ T helper cell response to dominant epitope peptide of major egg antigen Sm-p40.Experimental Parasitology90, 122–130. Granuloma formation in schistosomiasis is mediated by MHC class II-restricted CD4 + T helper lymphocytes sensitized to egg antigens. We previously reported that C3H mice, which develop large granulomas, display strong CD4 + T helper cell responses to the major egg antigen Sm-p40. Moreover, all members of a panel of egg antigen-specific T cell hybridomas responded to the Sm-p40 antigen. Given the significance of the Sm-p40 molecule in the C3H T cell repertoire against schistosomal egg antigens, the current work was undertaken to map its immunogenic epitopes, using a library of 15 synthetic overlapping 30-mer peptides. The dominant epitope recognized by polyclonal CD4 + Th cells was located in peptide 10 (amino acids 229–258); subdominant epitopes were detected in peptides 8 (amino acids 179–208) and 12 (amino acids 279–308). The anti-Sm-p40 T cell hybridomas variously responded to any one of the same three stimulatory peptides. Furthermore, studies with various mouse strains demonstrated that a strong anti-Sm-p40 response was restricted by H-2k. Interestingly, the cells responding to peptide 10 and to the Sm-p40 antigen only secreted IL-2 and IFN-γ, but not IL-4 and IL-10, indicating that they are entirely of the Th-1-type, a subset with demonstrated capacity to mediate egg granuloma formation. The identification of dominant epitopes within key egg antigens offers opportunities for desensitization of the CD4 + Th cells that mediate pathology in schistosomia sis.</abstract><qualityIndicators><refBibsNative>true</refBibsNative><abstractWordCount>268</abstractWordCount><abstractCharCount>1773</abstractCharCount><keywordCount>7</keywordCount><score>10</score><pdfWordCount>5542</pdfWordCount><pdfCharCount>33008</pdfCharCount><pdfVersion>1.2</pdfVersion><pdfPageCount>9</pdfPageCount><pdfPageSize>567 x 705 pts</pdfPageSize></qualityIndicators><title>Schistosoma mansoni: Genetic Restriction and Cytokine Profile of the CD4 + T Helper Cell Response to Dominant Epitope Peptide of Major Egg Antigen Sm-p40</title><pmid><json:string>9709038</json:string></pmid><pii><json:string>S0014-4894(98)94309-0</json:string></pii><genre><json:string>research-article</json:string></genre><host><title>Experimental Parasitology</title><language><json:string>unknown</json:string></language><publicationDate>1998</publicationDate><issn><json:string>0014-4894</json:string></issn><pii><json:string>S0014-4894(00)X0043-4</json:string></pii><volume>90</volume><issue>1</issue><pages><first>122</first><last>130</last></pages><genre><json:string>journal</json:string></genre></host><namedEntities><unitex><date><json:string>1998</json:string></date><geogName></geogName><orgName><json:string>World Bank</json:string><json:string>Research and Training</json:string><json:string>Department of Biological Molecular Pharmacology, Harvard Medical School, Boston, Massachusetts</json:string><json:string>University of Massachusetts</json:string><json:string>American Journal of Tropical Medicine and Hygiene</json:string><json:string>Department of Tropical Public Health, Harvard School of Public Health, Boston, Massachusetts</json:string><json:string>Biomedical Research Institute</json:string><json:string>U</json:string></orgName><orgName_funder><json:string>U</json:string></orgName_funder><orgName_provider></orgName_provider><persName><json:string>Schistosoma</json:string><json:string>U.S.A. Hernandez</json:string><json:string>Jackson Laboratory</json:string><json:string>Hector J. Hernandez</json:string><json:string>Miguel J. Stadecker</json:string><json:string>Donald A. Harn</json:string><json:string>Diana Pierce</json:string><json:string>John Cordingley</json:string><json:string>Clark M. Edson</json:string><json:string>Christopher J. Ianelli</json:string><json:string>Wendy Trzyna</json:string><json:string>Charles Dahl</json:string></persName><placeName><json:string>San Diego</json:string><json:string>MD</json:string><json:string>Rockville</json:string><json:string>CA</json:string><json:string>Kanazawa</json:string></placeName><ref_url></ref_url><ref_bibl><json:string>Bancroft et al. 1994</json:string><json:string>Kakimi et al. 1995</json:string><json:string>Sartono et al. 1996</json:string><json:string>Robinson et al. 1993</json:string><json:string>White et al. 1989</json:string><json:string>Weiss and Strand 1985</json:string><json:string>Haberman et al. 1990</json:string><json:string>Senpuku et al. 1996</json:string><json:string>Bretscher et al. 1992</json:string><json:string>Wynn et al. 1993</json:string><json:string>Brown et al. 1977</json:string><json:string>Anton et al. 1995</json:string><json:string>Huygen et al. 1994</json:string><json:string>Harrison et al. 1979</json:string><json:string>Milich et al. 1995</json:string><json:string>Chikunguwo et al. 1993</json:string><json:string>Pelley et al. 1976</json:string><json:string>Carpino and Han 1972</json:string><json:string>Cai et al. 1996</json:string><json:string>Cheever et al. 1987</json:string><json:string>Harn et al. 1989</json:string><json:string>Schountz et al. 1996</json:string><json:string>Matthew and Boros 1986</json:string><json:string>Cao et al. 1993</json:string><json:string>Chikunguwo et al. 1991, 1993</json:string><json:string>Fanning et al. 1981</json:string><json:string>Hernandez et al. 1997b</json:string><json:string>Takahashi et al. 1996</json:string><json:string>Smithers and Doenhoff 1982</json:string><json:string>Al 18919</json:string><json:string>Chikunguwo et al. 1991</json:string><json:string>Nicholson et al. 1995</json:string><json:string>Mosmann and Coffman 1989</json:string><json:string>Muir et al. 1994</json:string><json:string>Hernandez et al. 1997a</json:string><json:string>Lukacs and Boros 1991</json:string><json:string>Mohammadi et al. 1996</json:string><json:string>Pearce et al. 1991</json:string><json:string>Boros 1989</json:string><json:string>Boros and Warren 1970</json:string><json:string>Safley et al. 1995</json:string><json:string>Ogawa et al. 1995</json:string><json:string>Bhardwaj et al. 1992</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/6H6-80ZH2CVW-G</json:string></ark><categories><wos><json:string>1 - science</json:string><json:string>2 - parasitology</json:string></wos><scienceMetrix><json:string>1 - health sciences</json:string><json:string>2 - biomedical research</json:string><json:string>3 - mycology & parasitology</json:string></scienceMetrix><scopus><json:string>1 - Life Sciences</json:string><json:string>2 - Immunology and Microbiology</json:string><json:string>3 - Immunology</json:string><json:string>1 - Health Sciences</json:string><json:string>2 - Medicine</json:string><json:string>3 - General Medicine</json:string><json:string>1 - Life Sciences</json:string><json:string>2 - Immunology and Microbiology</json:string><json:string>3 - Parasitology</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 biologiques fondamentales et appliquees. psychologie</json:string></inist></categories><publicationDate>1998</publicationDate><copyrightDate>1998</copyrightDate><doi><json:string>10.1006/expr.1998.4309</json:string></doi><id>E6F16FE72E07A87A2C260BEE903363C126A35D13</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-80ZH2CVW-G/fulltext.pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-80ZH2CVW-G/bundle.zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/ark:/67375/6H6-80ZH2CVW-G/fulltext.tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Schistosoma mansoni: Genetic Restriction and Cytokine Profile of the CD4 + T Helper Cell Response to Dominant Epitope Peptide of Major Egg Antigen Sm-p40</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>We thank Drs. Wendy Trzyna and John Cordingley for providing the rSm-p40 clones and Diana Pierce for expert editorial assistance. This work was supported in part by grants from the U.S. Public Health Service (Al 18919) and from the UNDP/World Bank WHO Special Programme for Research and Training in Tropical Diseases to M.J.S.</note><note>S. CohenK. S. Warren</note><note type="content">Section title: Regular Article</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Schistosoma mansoni: Genetic Restriction and Cytokine Profile of the CD4 + T Helper Cell Response to Dominant Epitope Peptide of Major Egg Antigen Sm-p40</title><author xml:id="author-0000"><persName><forename type="first">Hector J.</forename><surname>Hernandez</surname></persName><affiliation>Department of Pathology, Tufts University School of Medicine, Boston, Massachusetts, 02111, U.S.A.</affiliation></author><author xml:id="author-0001"><persName><forename type="first">Clark M.</forename><surname>Edson</surname></persName><affiliation>Department of Pathology, Tufts University School of Medicine, Boston, Massachusetts, 02111, U.S.A.</affiliation></author><author xml:id="author-0002"><persName><forename type="first">Donald A.</forename><surname>Harn</surname></persName><affiliation>Department of Tropical Public Health, Harvard School of Public Health, Boston, Massachusetts, 02115, U.S.A.</affiliation></author><author xml:id="author-0003"><persName><forename type="first">Christopher J.</forename><surname>Ianelli</surname></persName><affiliation>Department of Pathology, Tufts University School of Medicine, Boston, Massachusetts, 02111, U.S.A.</affiliation></author><author xml:id="author-0004"><persName><forename type="first">Miguel J.</forename><surname>Stadecker</surname></persName><affiliation>Department of Pathology, Tufts University School of Medicine, Boston, Massachusetts, 02111, U.S.A.</affiliation></author><idno type="istex">E6F16FE72E07A87A2C260BEE903363C126A35D13</idno><idno type="ark">ark:/67375/6H6-80ZH2CVW-G</idno><idno type="DOI">10.1006/expr.1998.4309</idno><idno type="PII">S0014-4894(98)94309-0</idno></analytic><monogr><title level="j">Experimental Parasitology</title><title level="j" type="abbrev">YEXPR</title><idno type="pISSN">0014-4894</idno><idno type="PII">S0014-4894(00)X0043-4</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1998"></date><biblScope unit="volume">90</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="122">122</biblScope><biblScope unit="page" to="130">130</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: Hernandez, H. J., Edson, C. M., Harn, D. A., Ianelli, C. J., and Stadecker, M. J. 1998.Schistosoma mansoni: Genetic restriction and cytokine profile of the CD4+ T helper cell response to dominant epitope peptide of major egg antigen Sm-p40.Experimental Parasitology90, 122–130. Granuloma formation in schistosomiasis is mediated by MHC class II-restricted CD4 + T helper lymphocytes sensitized to egg antigens. We previously reported that C3H mice, which develop large granulomas, display strong CD4 + T helper cell responses to the major egg antigen Sm-p40. Moreover, all members of a panel of egg antigen-specific T cell hybridomas responded to the Sm-p40 antigen. Given the significance of the Sm-p40 molecule in the C3H T cell repertoire against schistosomal egg antigens, the current work was undertaken to map its immunogenic epitopes, using a library of 15 synthetic overlapping 30-mer peptides. The dominant epitope recognized by polyclonal CD4 + Th cells was located in peptide 10 (amino acids 229–258); subdominant epitopes were detected in peptides 8 (amino acids 179–208) and 12 (amino acids 279–308). The anti-Sm-p40 T cell hybridomas variously responded to any one of the same three stimulatory peptides. Furthermore, studies with various mouse strains demonstrated that a strong anti-Sm-p40 response was restricted by H-2k. Interestingly, the cells responding to peptide 10 and to the Sm-p40 antigen only secreted IL-2 and IFN-γ, but not IL-4 and IL-10, indicating that they are entirely of the Th-1-type, a subset with demonstrated capacity to mediate egg granuloma formation. The identification of dominant epitopes within key egg antigens offers opportunities for desensitization of the CD4 + Th cells that mediate pathology in schistosomia sis.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Abbreviations</head><item><term>Schistosoma mansoni</term></item><item><term>egg antigens</term></item><item><term>T cell epitopes</term></item><item><term>T cell subsets</term></item><item><term>MHC restriction</term></item><item><term>cytokines</term></item><item><term>SEA, schistosomal egg antigens.</term></item></list></keywords></textClass></profileDesc><revisionDesc><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:/67375/6H6-80ZH2CVW-G/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>YEXPR</jid><aid>94309</aid><ce:pii>S0014-4894(98)94309-0</ce:pii><ce:doi>10.1006/expr.1998.4309</ce:doi><ce:copyright type="full-transfer" year="1998">Academic Press</ce:copyright></item-info><head><ce:article-footnote><ce:label>☆</ce:label><ce:note-para>We thank Drs. Wendy Trzyna and John Cordingley for providing the rSm-p40 clones and Diana Pierce for expert editorial assistance. This work was supported in part by grants from the U.S. Public Health Service (Al 18919) and from the UNDP/World Bank WHO Special Programme for Research and Training in Tropical Diseases to M.J.S.</ce:note-para></ce:article-footnote><ce:article-footnote><ce:label>☆☆</ce:label><ce:note-para>S. CohenK. S. Warren</ce:note-para></ce:article-footnote><ce:dochead><ce:textfn>Regular Article</ce:textfn></ce:dochead><ce:title><ce:italic>Schistosoma mansoni:</ce:italic>Genetic Restriction and Cytokine Profile of the CD4 + T Helper Cell Response to Dominant Epitope Peptide of Major Egg Antigen Sm-p40</ce:title><ce:author-group><ce:author><ce:given-name>Hector J.</ce:given-name><ce:surname>Hernandez</ce:surname><ce:cross-ref refid="PR984309A1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Clark M.</ce:given-name><ce:surname>Edson</ce:surname><ce:cross-ref refid="PR984309A1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Donald A.</ce:given-name><ce:surname>Harn</ce:surname><ce:cross-ref refid="PR984309A2"><ce:sup>b</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Christopher J.</ce:given-name><ce:surname>Ianelli</ce:surname><ce:cross-ref refid="PR984309A1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Miguel J.</ce:given-name><ce:surname>Stadecker</ce:surname><ce:cross-ref refid="PR984309A1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:affiliation id="PR984309A1"><ce:label>a</ce:label><ce:textfn>Department of Pathology, Tufts University School of Medicine, Boston, Massachusetts, 02111, U.S.A.</ce:textfn></ce:affiliation><ce:affiliation id="PR984309A2"><ce:label>b</ce:label><ce:textfn>Department of Tropical Public Health, Harvard School of Public Health, Boston, Massachusetts, 02115, U.S.A.</ce:textfn></ce:affiliation></ce:author-group><ce:date-received day="6" month="2" year="1998"></ce:date-received><ce:date-accepted day="3" month="4" year="1998"></ce:date-accepted><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>Hernandez, H. J., Edson, C. M., Harn, D. A., Ianelli, C. J., and Stadecker, M. J. 1998.<ce:italic>Schistosoma mansoni</ce:italic>: Genetic restriction and cytokine profile of the CD4+ T helper cell response to dominant epitope peptide of major egg antigen Sm-p40.<ce:italic>Experimental Parasitology</ce:italic><ce:bold>90</ce:bold>, 122–130. Granuloma formation in schistosomiasis is mediated by MHC class II-restricted CD4 + T helper lymphocytes sensitized to egg antigens. We previously reported that C3H mice, which develop large granulomas, display strong CD4 + T helper cell responses to the major egg antigen Sm-p40. Moreover, all members of a panel of egg antigen-specific T cell hybridomas responded to the Sm-p40 antigen. Given the significance of the Sm-p40 molecule in the C3H T cell repertoire against schistosomal egg antigens, the current work was undertaken to map its immunogenic epitopes, using a library of 15 synthetic overlapping 30-mer peptides. The dominant epitope recognized by polyclonal CD4 + Th cells was located in peptide 10 (amino acids 229–258); subdominant epitopes were detected in peptides 8 (amino acids 179–208) and 12 (amino acids 279–308). The anti-Sm-p40 T cell hybridomas variously responded to any one of the same three stimulatory peptides. Furthermore, studies with various mouse strains demonstrated that a strong anti-Sm-p40 response was restricted by H-2<ce:sup>k</ce:sup>. Interestingly, the cells responding to peptide 10 and to the Sm-p40 antigen only secreted IL-2 and IFN-γ, but not IL-4 and IL-10, indicating that they are entirely of the Th-1-type, a subset with demonstrated capacity to mediate egg granuloma formation. The identification of dominant epitopes within key egg antigens offers opportunities for desensitization of the CD4 + Th cells that mediate pathology in schistosomia sis.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords class="abr"><ce:section-title>Abbreviations</ce:section-title><ce:keyword><ce:text><ce:italic>Schistosoma mansoni</ce:italic></ce:text></ce:keyword><ce:keyword><ce:text>egg antigens</ce:text></ce:keyword><ce:keyword><ce:text>T cell epitopes</ce:text></ce:keyword><ce:keyword><ce:text>T cell subsets</ce:text></ce:keyword><ce:keyword><ce:text>MHC restriction</ce:text></ce:keyword><ce:keyword><ce:text>cytokines</ce:text></ce:keyword><ce:keyword><ce:text>SEA, schistosomal egg antigens.</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Schistosoma mansoni: Genetic Restriction and Cytokine Profile of the CD4 + T Helper Cell Response to Dominant Epitope Peptide of Major Egg Antigen Sm-p40</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Genetic Restriction and Cytokine Profile of the CD4 + T Helper Cell Response to Dominant Epitope Peptide of Major Egg Antigen Sm-p40</title></titleInfo><name type="personal"><namePart type="given">Hector J.</namePart><namePart type="family">Hernandez</namePart><affiliation>Department of Pathology, Tufts University School of Medicine, Boston, Massachusetts, 02111, U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Clark M.</namePart><namePart type="family">Edson</namePart><affiliation>Department of Pathology, Tufts University School of Medicine, Boston, Massachusetts, 02111, U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Donald A.</namePart><namePart type="family">Harn</namePart><affiliation>Department of Tropical Public Health, Harvard School of Public Health, Boston, Massachusetts, 02115, U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Christopher J.</namePart><namePart type="family">Ianelli</namePart><affiliation>Department of Pathology, Tufts University School of Medicine, Boston, Massachusetts, 02111, U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Miguel J.</namePart><namePart type="family">Stadecker</namePart><affiliation>Department of Pathology, Tufts University School of Medicine, Boston, Massachusetts, 02111, U.S.A.</affiliation><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><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: Hernandez, H. J., Edson, C. M., Harn, D. A., Ianelli, C. J., and Stadecker, M. J. 1998.Schistosoma mansoni: Genetic restriction and cytokine profile of the CD4+ T helper cell response to dominant epitope peptide of major egg antigen Sm-p40.Experimental Parasitology90, 122–130. Granuloma formation in schistosomiasis is mediated by MHC class II-restricted CD4 + T helper lymphocytes sensitized to egg antigens. We previously reported that C3H mice, which develop large granulomas, display strong CD4 + T helper cell responses to the major egg antigen Sm-p40. Moreover, all members of a panel of egg antigen-specific T cell hybridomas responded to the Sm-p40 antigen. Given the significance of the Sm-p40 molecule in the C3H T cell repertoire against schistosomal egg antigens, the current work was undertaken to map its immunogenic epitopes, using a library of 15 synthetic overlapping 30-mer peptides. The dominant epitope recognized by polyclonal CD4 + Th cells was located in peptide 10 (amino acids 229–258); subdominant epitopes were detected in peptides 8 (amino acids 179–208) and 12 (amino acids 279–308). The anti-Sm-p40 T cell hybridomas variously responded to any one of the same three stimulatory peptides. Furthermore, studies with various mouse strains demonstrated that a strong anti-Sm-p40 response was restricted by H-2k. Interestingly, the cells responding to peptide 10 and to the Sm-p40 antigen only secreted IL-2 and IFN-γ, but not IL-4 and IL-10, indicating that they are entirely of the Th-1-type, a subset with demonstrated capacity to mediate egg granuloma formation. The identification of dominant epitopes within key egg antigens offers opportunities for desensitization of the CD4 + Th cells that mediate pathology in schistosomia sis.</abstract><note>We thank Drs. Wendy Trzyna and John Cordingley for providing the rSm-p40 clones and Diana Pierce for expert editorial assistance. This work was supported in part by grants from the U.S. Public Health Service (Al 18919) and from the UNDP/World Bank WHO Special Programme for Research and Training in Tropical Diseases to M.J.S.</note><note>S. CohenK. S. Warren</note><note type="content">Section title: Regular Article</note><subject lang="en"><genre>Abbreviations</genre><topic>Schistosoma mansoni</topic><topic>egg antigens</topic><topic>T cell epitopes</topic><topic>T cell subsets</topic><topic>MHC restriction</topic><topic>cytokines</topic><topic>SEA, schistosomal egg antigens.</topic></subject><relatedItem type="host"><titleInfo><title>Experimental Parasitology</title></titleInfo><titleInfo type="abbreviated"><title>YEXPR</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">0014-4894</identifier><identifier type="PII">S0014-4894(00)X0043-4</identifier><part><date>1998</date><detail type="volume"><number>90</number><caption>vol.</caption></detail><detail type="issue"><number>1</number><caption>no.</caption></detail><extent unit="issue-pages"><start>1</start><end>141</end></extent><extent unit="pages"><start>122</start><end>130</end></extent></part></relatedItem><identifier type="istex">E6F16FE72E07A87A2C260BEE903363C126A35D13</identifier><identifier type="ark">ark:/67375/6H6-80ZH2CVW-G</identifier><identifier type="DOI">10.1006/expr.1998.4309</identifier><identifier type="PII">S0014-4894(98)94309-0</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:/67375/6H6-80ZH2CVW-G/record.json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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