Identification of an HLA-A*0201-restricted CD8+ T-cell epitope SSp- 1 of SARS-CoV spike protein
Identifieur interne : 000769 ( PascalFrancis/Corpus ); précédent : 000768; suivant : 000770Identification of an HLA-A*0201-restricted CD8+ T-cell epitope SSp- 1 of SARS-CoV spike protein
Auteurs : BAOMEI WANG ; HUABIAO CHEN ; XIAODONG JIANG ; MINGHUI ZHANG ; TAO WAN ; NAN LI ; XIANGYANG ZHOU ; YANFENG WU ; FENG YANG ; YIZHI YU ; XIAONING WANG ; RUIFU YANG ; XUETAO CAOSource :
- Blood [ 0006-4971 ] ; 2004.
Descripteurs français
- Pascal (Inist)
- Syndrome respiratoire aigu sévère, Coronavirus, Glycoprotéine, Déterminant antigénique, Peptide, Système histocompatibilité majeur, Système HLA, Antigène histocompatibilité classe I, Locus HLA-A, Restriction histocompatibilité, Lymphocyte T, Lymphocyte T cytotoxique, Réponse immune, Animal transgénique, Souris, Antigène CD8, Protéine SSp-1.
English descriptors
- KwdEn :
- Antigenic determinant, Class I histocompatibility antigen, Coronavirus, Cytotoxic T lymphocyte, Glycoprotein, HLA-A-Locus, HLA-System, Histocompatibility restriction, Immune response, Major histocompatibility system, Mouse, Peptides, Severe acute respiratory syndrome, T-Lymphocyte, Transgenic animal.
Abstract
A novel coronavirus, severe acute respiratory syndrome (SARS)-associated coronavirus (SARS-CoV), has been identified as the causal agent of SARS. Spike (S) protein is a major structural glycoprotein of the SARS virus and a potential target for SARS-specific cell-mediated immune responses. A panel of S protein-derived peptides was tested for their binding affinity to HLA-A*0201 molecules. Peptides with high affinity for HLA-A*0201 were then assessed for their capacity to elicit specific immune responses mediated by cytotoxic T lymphocytes (CTLs) both in vivo, in HLA-A2.1/Kb transgenic mice, and in vitro, from peripheral blood lymphocytes (PBLs) sourced from healthy HLA-A2.1+ donors. SARS-CoV protein-derived peptide-1 (SSp-1 RLNEVAKNL), induced peptide-specific CTLs both in vivo (transgenic mice) and in vitro (human PBLs), which specifically released interferon-γ (IFN-γ) upon stimulation with SSp-1-pulsed autologous dendritic cells (DCs) or T2 cells. SSp-1-specific CTLs also lysed major histocompatibility complex (MHC)-matched tumor cell lines engineered to express S proteins. HLA-A*0201-SSp-1 tetramer staining revealed the presence of significant populations of SSp-1-specific CTLs in SSp-1-induced CD8+ T cells. We propose that the newly identified epitope SSp-1 will help in the characterization of virus control mechanisms and immunopathology in SARS-CoV infection, and may be relevant to the development of immunotherapeutic approaches for SARS.
Notice en format standard (ISO 2709)
Pour connaître la documentation sur le format Inist Standard.
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Format Inist (serveur)
| NO : | PASCAL 04-0586081 INIST |
|---|---|
| ET : | Identification of an HLA-A*0201-restricted CD8+ T-cell epitope SSp- 1 of SARS-CoV spike protein |
| AU : | BAOMEI WANG; HUABIAO CHEN; XIAODONG JIANG; MINGHUI ZHANG; TAO WAN; NAN LI; XIANGYANG ZHOU; YANFENG WU; FENG YANG; YIZHI YU; XIAONING WANG; RUIFU YANG; XUETAO CAO |
| AF : | Institute of Immunology, Second Military Medical University/Shanghai/Chine; Institute of Immunology, Zhejiang University/Hangzhou/Chine; Institute of Molecular Immunology, First Military Medical University/Guangzhou/Chine; Institute of Microbiology and Epidemiology, Chinese Academy of Military Medical Sciences/Beijing/Chine |
| DT : | Publication en série; Niveau analytique |
| SO : | Blood; ISSN 0006-4971; Etats-Unis; Da. 2004; Vol. 104; No. 1; Pp. 200-206; Bibl. 67 ref. |
| LA : | Anglais |
| EA : | A novel coronavirus, severe acute respiratory syndrome (SARS)-associated coronavirus (SARS-CoV), has been identified as the causal agent of SARS. Spike (S) protein is a major structural glycoprotein of the SARS virus and a potential target for SARS-specific cell-mediated immune responses. A panel of S protein-derived peptides was tested for their binding affinity to HLA-A*0201 molecules. Peptides with high affinity for HLA-A*0201 were then assessed for their capacity to elicit specific immune responses mediated by cytotoxic T lymphocytes (CTLs) both in vivo, in HLA-A2.1/Kb transgenic mice, and in vitro, from peripheral blood lymphocytes (PBLs) sourced from healthy HLA-A2.1+ donors. SARS-CoV protein-derived peptide-1 (SSp-1 RLNEVAKNL), induced peptide-specific CTLs both in vivo (transgenic mice) and in vitro (human PBLs), which specifically released interferon-γ (IFN-γ) upon stimulation with SSp-1-pulsed autologous dendritic cells (DCs) or T2 cells. SSp-1-specific CTLs also lysed major histocompatibility complex (MHC)-matched tumor cell lines engineered to express S proteins. HLA-A*0201-SSp-1 tetramer staining revealed the presence of significant populations of SSp-1-specific CTLs in SSp-1-induced CD8+ T cells. We propose that the newly identified epitope SSp-1 will help in the characterization of virus control mechanisms and immunopathology in SARS-CoV infection, and may be relevant to the development of immunotherapeutic approaches for SARS. |
| CC : | 002B05C02C |
| FD : | Syndrome respiratoire aigu sévère; Coronavirus; Glycoprotéine; Déterminant antigénique; Peptide; Système histocompatibilité majeur; Système HLA; Antigène histocompatibilité classe I; Locus HLA-A; Restriction histocompatibilité; Lymphocyte T; Lymphocyte T cytotoxique; Réponse immune; Animal transgénique; Souris; Antigène CD8; Protéine SSp-1 |
| FG : | Virose; Infection; Coronaviridae; Nidovirales; Virus; Rodentia; Mammalia; Vertebrata |
| ED : | Severe acute respiratory syndrome; Coronavirus; Glycoprotein; Antigenic determinant; Peptides; Major histocompatibility system; HLA-System; Class I histocompatibility antigen; HLA-A-Locus; Histocompatibility restriction; T-Lymphocyte; Cytotoxic T lymphocyte; Immune response; Transgenic animal; Mouse |
| EG : | Viral disease; Infection; Coronaviridae; Nidovirales; Virus; Rodentia; Mammalia; Vertebrata |
| SD : | Síndrome respiratorio agudo severo; Coronavirus; Glicoproteína; Determinante antigénico; Péptido; Sistema histocompatibilidad mayor; Sistema HLA; Antígeno histocompatibilidad clase I; Locus HLA-A; Restricción histocompatibilidad; Linfocito T; Linfocito T citotóxico; Respuesta inmune; Animal transgénico; Ratón |
| LO : | INIST-3178.354000113878430280 |
| ID : | 04-0586081 |
Links to Exploration step
Pascal:04-0586081Le document en format XML
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sort="Huabiao Chen" uniqKey="Huabiao Chen" last="Huabiao Chen">HUABIAO CHEN</name></author><author><name sortKey="Xiaodong Jiang" sort="Xiaodong Jiang" uniqKey="Xiaodong Jiang" last="Xiaodong Jiang">XIAODONG JIANG</name></author><author><name sortKey="Minghui Zhang" sort="Minghui Zhang" uniqKey="Minghui Zhang" last="Minghui Zhang">MINGHUI ZHANG</name></author><author><name sortKey="Tao Wan" sort="Tao Wan" uniqKey="Tao Wan" last="Tao Wan">TAO WAN</name></author><author><name sortKey="Nan Li" sort="Nan Li" uniqKey="Nan Li" last="Nan Li">NAN LI</name></author><author><name sortKey="Xiangyang Zhou" sort="Xiangyang Zhou" uniqKey="Xiangyang Zhou" last="Xiangyang Zhou">XIANGYANG ZHOU</name></author><author><name sortKey="Yanfeng Wu" sort="Yanfeng Wu" uniqKey="Yanfeng Wu" last="Yanfeng Wu">YANFENG WU</name></author><author><name sortKey="Feng Yang" sort="Feng Yang" uniqKey="Feng Yang" last="Feng Yang">FENG YANG</name></author><author><name sortKey="Yizhi Yu" sort="Yizhi Yu" uniqKey="Yizhi Yu" last="Yizhi Yu">YIZHI YU</name></author><author><name sortKey="Xiaoning Wang" sort="Xiaoning Wang" uniqKey="Xiaoning Wang" last="Xiaoning Wang">XIAONING WANG</name></author><author><name sortKey="Ruifu Yang" sort="Ruifu Yang" uniqKey="Ruifu Yang" last="Ruifu Yang">RUIFU YANG</name></author><author><name sortKey="Xuetao Cao" sort="Xuetao Cao" uniqKey="Xuetao Cao" last="Xuetao Cao">XUETAO CAO</name></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">04-0586081</idno><date when="2004">2004</date><idno type="stanalyst">PASCAL 04-0586081 INIST</idno><idno type="RBID">Pascal:04-0586081</idno><idno type="wicri:Area/PascalFrancis/Corpus">000769</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Identification of an HLA-A*0201-restricted CD8<sup>+</sup> T-cell epitope SSp- 1 of SARS-CoV spike protein</title><author><name sortKey="Baomei Wang" sort="Baomei Wang" uniqKey="Baomei Wang" last="Baomei Wang">BAOMEI WANG</name><affiliation><inist:fA14 i1="01"><s1>Institute of Immunology, Second Military Medical University</s1><s2>Shanghai</s2><s3>CHN</s3></inist:fA14></affiliation><affiliation><inist:fA14 i1="02"><s1>Institute of Immunology, Zhejiang University</s1><s2>Hangzhou</s2><s3>CHN</s3></inist:fA14></affiliation><affiliation><inist:fA14 i1="03"><s1>Institute of Molecular Immunology, First Military Medical University</s1><s2>Guangzhou</s2><s3>CHN</s3></inist:fA14></affiliation><affiliation><inist:fA14 i1="04"><s1>Institute of Microbiology and Epidemiology, Chinese Academy of Military Medical Sciences</s1><s2>Beijing</s2><s3>CHN</s3></inist:fA14></affiliation></author><author><name sortKey="Huabiao Chen" sort="Huabiao Chen" uniqKey="Huabiao Chen" last="Huabiao Chen">HUABIAO CHEN</name></author><author><name sortKey="Xiaodong Jiang" sort="Xiaodong Jiang" uniqKey="Xiaodong Jiang" last="Xiaodong Jiang">XIAODONG JIANG</name></author><author><name sortKey="Minghui Zhang" sort="Minghui Zhang" uniqKey="Minghui Zhang" last="Minghui Zhang">MINGHUI ZHANG</name></author><author><name sortKey="Tao Wan" sort="Tao Wan" uniqKey="Tao Wan" last="Tao Wan">TAO WAN</name></author><author><name sortKey="Nan Li" sort="Nan Li" uniqKey="Nan Li" last="Nan Li">NAN LI</name></author><author><name sortKey="Xiangyang Zhou" sort="Xiangyang Zhou" uniqKey="Xiangyang Zhou" last="Xiangyang Zhou">XIANGYANG ZHOU</name></author><author><name sortKey="Yanfeng Wu" sort="Yanfeng Wu" uniqKey="Yanfeng Wu" last="Yanfeng Wu">YANFENG WU</name></author><author><name sortKey="Feng Yang" sort="Feng Yang" uniqKey="Feng Yang" last="Feng Yang">FENG YANG</name></author><author><name sortKey="Yizhi Yu" sort="Yizhi Yu" uniqKey="Yizhi Yu" last="Yizhi Yu">YIZHI YU</name></author><author><name sortKey="Xiaoning Wang" sort="Xiaoning Wang" uniqKey="Xiaoning Wang" last="Xiaoning Wang">XIAONING WANG</name></author><author><name sortKey="Ruifu Yang" sort="Ruifu Yang" uniqKey="Ruifu Yang" last="Ruifu Yang">RUIFU YANG</name></author><author><name sortKey="Xuetao Cao" sort="Xuetao Cao" uniqKey="Xuetao Cao" last="Xuetao Cao">XUETAO CAO</name></author></analytic><series><title level="j" type="main">Blood</title><title level="j" type="abbreviated">Blood</title><idno type="ISSN">0006-4971</idno><imprint><date when="2004">2004</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Blood</title><title level="j" type="abbreviated">Blood</title><idno type="ISSN">0006-4971</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antigenic determinant</term><term>Class I histocompatibility antigen</term><term>Coronavirus</term><term>Cytotoxic T lymphocyte</term><term>Glycoprotein</term><term>HLA-A-Locus</term><term>HLA-System</term><term>Histocompatibility restriction</term><term>Immune response</term><term>Major histocompatibility system</term><term>Mouse</term><term>Peptides</term><term>Severe acute respiratory syndrome</term><term>T-Lymphocyte</term><term>Transgenic animal</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Syndrome respiratoire aigu sévère</term><term>Coronavirus</term><term>Glycoprotéine</term><term>Déterminant antigénique</term><term>Peptide</term><term>Système histocompatibilité majeur</term><term>Système HLA</term><term>Antigène histocompatibilité classe I</term><term>Locus HLA-A</term><term>Restriction histocompatibilité</term><term>Lymphocyte T</term><term>Lymphocyte T cytotoxique</term><term>Réponse immune</term><term>Animal transgénique</term><term>Souris</term><term>Antigène CD8</term><term>Protéine SSp-1</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">A novel coronavirus, severe acute respiratory syndrome (SARS)-associated coronavirus (SARS-CoV), has been identified as the causal agent of SARS. Spike (S) protein is a major structural glycoprotein of the SARS virus and a potential target for SARS-specific cell-mediated immune responses. A panel of S protein-derived peptides was tested for their binding affinity to HLA-A*0201 molecules. Peptides with high affinity for HLA-A*0201 were then assessed for their capacity to elicit specific immune responses mediated by cytotoxic T lymphocytes (CTLs) both in vivo, in HLA-A2.1/K<sup>b</sup> transgenic mice, and in vitro, from peripheral blood lymphocytes (PBLs) sourced from healthy HLA-A2.1<sup>+</sup> donors. SARS-CoV protein-derived peptide-1 (SSp-1 RLNEVAKNL), induced peptide-specific CTLs both in vivo (transgenic mice) and in vitro (human PBLs), which specifically released interferon-γ (IFN-γ) upon stimulation with SSp-1-pulsed autologous dendritic cells (DCs) or T2 cells. SSp-1-specific CTLs also lysed major histocompatibility complex (MHC)-matched tumor cell lines engineered to express S proteins. HLA-A*0201-SSp-1 tetramer staining revealed the presence of significant populations of SSp-1-specific CTLs in SSp-1-induced CD8<sup>+</sup> T cells. We propose that the newly identified epitope SSp-1 will help in the characterization of virus control mechanisms and immunopathology in SARS-CoV infection, and may be relevant to the development of immunotherapeutic approaches for SARS.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0006-4971</s0></fA01><fA03 i2="1"><s0>Blood</s0></fA03><fA05><s2>104</s2></fA05><fA06><s2>1</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Identification of an HLA-A*0201-restricted CD8<sup>+</sup> T-cell epitope SSp- 1 of SARS-CoV spike protein</s1></fA08><fA11 i1="01" i2="1"><s1>BAOMEI WANG</s1></fA11><fA11 i1="02" i2="1"><s1>HUABIAO CHEN</s1></fA11><fA11 i1="03" i2="1"><s1>XIAODONG JIANG</s1></fA11><fA11 i1="04" i2="1"><s1>MINGHUI ZHANG</s1></fA11><fA11 i1="05" i2="1"><s1>TAO WAN</s1></fA11><fA11 i1="06" i2="1"><s1>NAN LI</s1></fA11><fA11 i1="07" i2="1"><s1>XIANGYANG ZHOU</s1></fA11><fA11 i1="08" i2="1"><s1>YANFENG WU</s1></fA11><fA11 i1="09" i2="1"><s1>FENG YANG</s1></fA11><fA11 i1="10" i2="1"><s1>YIZHI YU</s1></fA11><fA11 i1="11" i2="1"><s1>XIAONING WANG</s1></fA11><fA11 i1="12" i2="1"><s1>RUIFU YANG</s1></fA11><fA11 i1="13" i2="1"><s1>XUETAO CAO</s1></fA11><fA14 i1="01"><s1>Institute of Immunology, Second Military Medical University</s1><s2>Shanghai</s2><s3>CHN</s3></fA14><fA14 i1="02"><s1>Institute of Immunology, Zhejiang University</s1><s2>Hangzhou</s2><s3>CHN</s3></fA14><fA14 i1="03"><s1>Institute of Molecular Immunology, First Military Medical University</s1><s2>Guangzhou</s2><s3>CHN</s3></fA14><fA14 i1="04"><s1>Institute of Microbiology and Epidemiology, Chinese Academy of Military Medical Sciences</s1><s2>Beijing</s2><s3>CHN</s3></fA14><fA20><s1>200-206</s1></fA20><fA21><s1>2004</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>3178</s2><s5>354000113878430280</s5></fA43><fA44><s0>0000</s0><s1>© 2004 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>67 ref.</s0></fA45><fA47 i1="01" i2="1"><s0>04-0586081</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Blood</s0></fA64><fA66 i1="01"><s0>USA</s0></fA66><fC01 i1="01" l="ENG"><s0>A novel coronavirus, severe acute respiratory syndrome (SARS)-associated coronavirus (SARS-CoV), has been identified as the causal agent of SARS. Spike (S) protein is a major structural glycoprotein of the SARS virus and a potential target for SARS-specific cell-mediated immune responses. A panel of S protein-derived peptides was tested for their binding affinity to HLA-A*0201 molecules. Peptides with high affinity for HLA-A*0201 were then assessed for their capacity to elicit specific immune responses mediated by cytotoxic T lymphocytes (CTLs) both in vivo, in HLA-A2.1/K<sup>b</sup> transgenic mice, and in vitro, from peripheral blood lymphocytes (PBLs) sourced from healthy HLA-A2.1<sup>+</sup> donors. SARS-CoV protein-derived peptide-1 (SSp-1 RLNEVAKNL), induced peptide-specific CTLs both in vivo (transgenic mice) and in vitro (human PBLs), which specifically released interferon-γ (IFN-γ) upon stimulation with SSp-1-pulsed autologous dendritic cells (DCs) or T2 cells. SSp-1-specific CTLs also lysed major histocompatibility complex (MHC)-matched tumor cell lines engineered to express S proteins. HLA-A*0201-SSp-1 tetramer staining revealed the presence of significant populations of SSp-1-specific CTLs in SSp-1-induced CD8<sup>+</sup> T cells. We propose that the newly identified epitope SSp-1 will help in the characterization of virus control mechanisms and immunopathology in SARS-CoV infection, and may be relevant to the development of immunotherapeutic approaches for SARS.</s0></fC01><fC02 i1="01" i2="X"><s0>002B05C02C</s0></fC02><fC03 i1="01" i2="X" l="FRE"><s0>Syndrome respiratoire aigu sévère</s0><s2>NM</s2><s5>01</s5></fC03><fC03 i1="01" i2="X" l="ENG"><s0>Severe acute respiratory syndrome</s0><s2>NM</s2><s5>01</s5></fC03><fC03 i1="01" i2="X" l="SPA"><s0>Síndrome respiratorio agudo severo</s0><s2>NM</s2><s5>01</s5></fC03><fC03 i1="02" i2="X" l="FRE"><s0>Coronavirus</s0><s2>NW</s2><s5>02</s5></fC03><fC03 i1="02" i2="X" l="ENG"><s0>Coronavirus</s0><s2>NW</s2><s5>02</s5></fC03><fC03 i1="02" i2="X" l="SPA"><s0>Coronavirus</s0><s2>NW</s2><s5>02</s5></fC03><fC03 i1="03" i2="X" l="FRE"><s0>Glycoprotéine</s0><s5>03</s5></fC03><fC03 i1="03" i2="X" l="ENG"><s0>Glycoprotein</s0><s5>03</s5></fC03><fC03 i1="03" i2="X" l="SPA"><s0>Glicoproteína</s0><s5>03</s5></fC03><fC03 i1="04" i2="X" l="FRE"><s0>Déterminant antigénique</s0><s5>04</s5></fC03><fC03 i1="04" i2="X" l="ENG"><s0>Antigenic determinant</s0><s5>04</s5></fC03><fC03 i1="04" i2="X" l="SPA"><s0>Determinante antigénico</s0><s5>04</s5></fC03><fC03 i1="05" i2="X" l="FRE"><s0>Peptide</s0><s5>05</s5></fC03><fC03 i1="05" i2="X" l="ENG"><s0>Peptides</s0><s5>05</s5></fC03><fC03 i1="05" i2="X" l="SPA"><s0>Péptido</s0><s5>05</s5></fC03><fC03 i1="06" i2="X" l="FRE"><s0>Système histocompatibilité majeur</s0><s5>06</s5></fC03><fC03 i1="06" i2="X" l="ENG"><s0>Major histocompatibility system</s0><s5>06</s5></fC03><fC03 i1="06" i2="X" l="SPA"><s0>Sistema histocompatibilidad mayor</s0><s5>06</s5></fC03><fC03 i1="07" i2="X" l="FRE"><s0>Système HLA</s0><s5>07</s5></fC03><fC03 i1="07" i2="X" l="ENG"><s0>HLA-System</s0><s5>07</s5><s6>«HLA»-System</s6></fC03><fC03 i1="07" i2="X" l="SPA"><s0>Sistema HLA</s0><s5>07</s5></fC03><fC03 i1="08" i2="X" l="FRE"><s0>Antigène histocompatibilité classe I</s0><s5>08</s5></fC03><fC03 i1="08" i2="X" l="ENG"><s0>Class I histocompatibility antigen</s0><s5>08</s5></fC03><fC03 i1="08" i2="X" l="SPA"><s0>Antígeno histocompatibilidad clase I</s0><s5>08</s5></fC03><fC03 i1="09" i2="X" l="FRE"><s0>Locus HLA-A</s0><s5>09</s5></fC03><fC03 i1="09" i2="X" l="ENG"><s0>HLA-A-Locus</s0><s5>09</s5><s6>«HLA-A»-Locus</s6></fC03><fC03 i1="09" i2="X" l="SPA"><s0>Locus HLA-A</s0><s5>09</s5></fC03><fC03 i1="10" i2="X" l="FRE"><s0>Restriction histocompatibilité</s0><s5>10</s5></fC03><fC03 i1="10" i2="X" l="ENG"><s0>Histocompatibility restriction</s0><s5>10</s5></fC03><fC03 i1="10" i2="X" l="SPA"><s0>Restricción histocompatibilidad</s0><s5>10</s5></fC03><fC03 i1="11" i2="X" l="FRE"><s0>Lymphocyte T</s0><s5>11</s5></fC03><fC03 i1="11" i2="X" l="ENG"><s0>T-Lymphocyte</s0><s5>11</s5><s6>«T»-Lymphocyte</s6></fC03><fC03 i1="11" i2="X" l="SPA"><s0>Linfocito T</s0><s5>11</s5></fC03><fC03 i1="12" i2="X" l="FRE"><s0>Lymphocyte T cytotoxique</s0><s5>12</s5></fC03><fC03 i1="12" i2="X" l="ENG"><s0>Cytotoxic T lymphocyte</s0><s5>12</s5></fC03><fC03 i1="12" i2="X" l="SPA"><s0>Linfocito T citotóxico</s0><s5>12</s5></fC03><fC03 i1="13" i2="X" l="FRE"><s0>Réponse immune</s0><s5>13</s5></fC03><fC03 i1="13" i2="X" l="ENG"><s0>Immune response</s0><s5>13</s5></fC03><fC03 i1="13" i2="X" l="SPA"><s0>Respuesta inmune</s0><s5>13</s5></fC03><fC03 i1="14" i2="X" l="FRE"><s0>Animal transgénique</s0><s5>17</s5></fC03><fC03 i1="14" i2="X" l="ENG"><s0>Transgenic animal</s0><s5>17</s5></fC03><fC03 i1="14" i2="X" l="SPA"><s0>Animal transgénico</s0><s5>17</s5></fC03><fC03 i1="15" i2="X" l="FRE"><s0>Souris</s0><s5>18</s5></fC03><fC03 i1="15" i2="X" l="ENG"><s0>Mouse</s0><s5>18</s5></fC03><fC03 i1="15" i2="X" l="SPA"><s0>Ratón</s0><s5>18</s5></fC03><fC03 i1="16" i2="X" l="FRE"><s0>Antigène CD8</s0><s4>INC</s4><s5>86</s5></fC03><fC03 i1="17" i2="X" l="FRE"><s0>Protéine SSp-1</s0><s4>INC</s4><s5>87</s5></fC03><fC07 i1="01" i2="X" l="FRE"><s0>Virose</s0><s2>NM</s2></fC07><fC07 i1="01" i2="X" l="ENG"><s0>Viral disease</s0><s2>NM</s2></fC07><fC07 i1="01" i2="X" l="SPA"><s0>Virosis</s0><s2>NM</s2></fC07><fC07 i1="02" i2="X" l="FRE"><s0>Infection</s0><s2>NM</s2></fC07><fC07 i1="02" i2="X" l="ENG"><s0>Infection</s0><s2>NM</s2></fC07><fC07 i1="02" i2="X" l="SPA"><s0>Infección</s0><s2>NM</s2></fC07><fC07 i1="03" i2="X" l="FRE"><s0>Coronaviridae</s0><s2>NW</s2></fC07><fC07 i1="03" i2="X" l="ENG"><s0>Coronaviridae</s0><s2>NW</s2></fC07><fC07 i1="03" i2="X" l="SPA"><s0>Coronaviridae</s0><s2>NW</s2></fC07><fC07 i1="04" i2="X" l="FRE"><s0>Nidovirales</s0><s2>NW</s2></fC07><fC07 i1="04" i2="X" l="ENG"><s0>Nidovirales</s0><s2>NW</s2></fC07><fC07 i1="04" i2="X" l="SPA"><s0>Nidovirales</s0><s2>NW</s2></fC07><fC07 i1="05" i2="X" l="FRE"><s0>Virus</s0><s2>NW</s2></fC07><fC07 i1="05" i2="X" l="ENG"><s0>Virus</s0><s2>NW</s2></fC07><fC07 i1="05" i2="X" l="SPA"><s0>Virus</s0><s2>NW</s2></fC07><fC07 i1="06" i2="X" l="FRE"><s0>Rodentia</s0><s2>NS</s2></fC07><fC07 i1="06" i2="X" l="ENG"><s0>Rodentia</s0><s2>NS</s2></fC07><fC07 i1="06" i2="X" l="SPA"><s0>Rodentia</s0><s2>NS</s2></fC07><fC07 i1="07" i2="X" l="FRE"><s0>Mammalia</s0><s2>NS</s2></fC07><fC07 i1="07" i2="X" l="ENG"><s0>Mammalia</s0><s2>NS</s2></fC07><fC07 i1="07" i2="X" l="SPA"><s0>Mammalia</s0><s2>NS</s2></fC07><fC07 i1="08" i2="X" l="FRE"><s0>Vertebrata</s0><s2>NS</s2></fC07><fC07 i1="08" i2="X" l="ENG"><s0>Vertebrata</s0><s2>NS</s2></fC07><fC07 i1="08" i2="X" l="SPA"><s0>Vertebrata</s0><s2>NS</s2></fC07><fN21><s1>334</s1></fN21><fN44 i1="01"><s1>PSI</s1></fN44><fN82><s1>PSI</s1></fN82></pA></standard><server><NO>PASCAL 04-0586081 INIST</NO><ET>Identification of an HLA-A*0201-restricted CD8<sup>+</sup> T-cell epitope SSp- 1 of SARS-CoV spike protein</ET><AU>BAOMEI WANG; HUABIAO CHEN; XIAODONG JIANG; MINGHUI ZHANG; TAO WAN; NAN LI; XIANGYANG ZHOU; YANFENG WU; FENG YANG; YIZHI YU; XIAONING WANG; RUIFU YANG; XUETAO CAO</AU><AF>Institute of Immunology, Second Military Medical University/Shanghai/Chine; Institute of Immunology, Zhejiang University/Hangzhou/Chine; Institute of Molecular Immunology, First Military Medical University/Guangzhou/Chine; Institute of Microbiology and Epidemiology, Chinese Academy of Military Medical Sciences/Beijing/Chine</AF><DT>Publication en série; Niveau analytique</DT><SO>Blood; ISSN 0006-4971; Etats-Unis; Da. 2004; Vol. 104; No. 1; Pp. 200-206; Bibl. 67 ref.</SO><LA>Anglais</LA><EA>A novel coronavirus, severe acute respiratory syndrome (SARS)-associated coronavirus (SARS-CoV), has been identified as the causal agent of SARS. Spike (S) protein is a major structural glycoprotein of the SARS virus and a potential target for SARS-specific cell-mediated immune responses. A panel of S protein-derived peptides was tested for their binding affinity to HLA-A*0201 molecules. Peptides with high affinity for HLA-A*0201 were then assessed for their capacity to elicit specific immune responses mediated by cytotoxic T lymphocytes (CTLs) both in vivo, in HLA-A2.1/K<sup>b</sup> transgenic mice, and in vitro, from peripheral blood lymphocytes (PBLs) sourced from healthy HLA-A2.1<sup>+</sup> donors. SARS-CoV protein-derived peptide-1 (SSp-1 RLNEVAKNL), induced peptide-specific CTLs both in vivo (transgenic mice) and in vitro (human PBLs), which specifically released interferon-γ (IFN-γ) upon stimulation with SSp-1-pulsed autologous dendritic cells (DCs) or T2 cells. SSp-1-specific CTLs also lysed major histocompatibility complex (MHC)-matched tumor cell lines engineered to express S proteins. HLA-A*0201-SSp-1 tetramer staining revealed the presence of significant populations of SSp-1-specific CTLs in SSp-1-induced CD8<sup>+</sup> T cells. We propose that the newly identified epitope SSp-1 will help in the characterization of virus control mechanisms and immunopathology in SARS-CoV infection, and may be relevant to the development of immunotherapeutic approaches for SARS.</EA><CC>002B05C02C</CC><FD>Syndrome respiratoire aigu sévère; Coronavirus; Glycoprotéine; Déterminant antigénique; Peptide; Système histocompatibilité majeur; Système HLA; Antigène histocompatibilité classe I; Locus HLA-A; Restriction histocompatibilité; Lymphocyte T; Lymphocyte T cytotoxique; Réponse immune; Animal transgénique; Souris; Antigène CD8; Protéine SSp-1</FD><FG>Virose; Infection; Coronaviridae; Nidovirales; Virus; Rodentia; Mammalia; Vertebrata</FG><ED>Severe acute respiratory syndrome; Coronavirus; Glycoprotein; Antigenic determinant; Peptides; Major histocompatibility system; HLA-System; Class I histocompatibility antigen; HLA-A-Locus; Histocompatibility restriction; T-Lymphocyte; Cytotoxic T lymphocyte; Immune response; Transgenic animal; Mouse</ED><EG>Viral disease; Infection; Coronaviridae; Nidovirales; Virus; Rodentia; Mammalia; Vertebrata</EG><SD>Síndrome respiratorio agudo severo; Coronavirus; Glicoproteína; Determinante antigénico; Péptido; Sistema histocompatibilidad mayor; Sistema HLA; Antígeno histocompatibilidad clase I; Locus HLA-A; Restricción histocompatibilidad; Linfocito T; Linfocito T citotóxico; Respuesta inmune; Animal transgénico; Ratón</SD><LO>INIST-3178.354000113878430280</LO><ID>04-0586081</ID></server></inist></record>Pour manipuler ce document sous Unix (Dilib)
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