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Identification of an HLA-A*0201-restricted CD8+ T-cell epitope SSp- 1 of SARS-CoV spike protein

Identifieur interne : 000221 ( PascalFrancis/Curation ); précédent : 000220; suivant : 000222

Identification of an HLA-A*0201-restricted CD8+ T-cell epitope SSp- 1 of SARS-CoV spike protein

Auteurs : BAOMEI WANG [République populaire de Chine] ; HUABIAO CHEN ; XIAODONG JIANG ; MINGHUI ZHANG ; TAO WAN ; NAN LI ; XIANGYANG ZHOU ; YANFENG WU ; FENG YANG ; YIZHI YU ; XIAONING WANG ; RUIFU YANG ; XUETAO CAO

Source :

RBID : Pascal:04-0586081

Descripteurs français

English descriptors

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.
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A11 02  1    @1 HUABIAO CHEN
A11 03  1    @1 XIAODONG JIANG
A11 04  1    @1 MINGHUI ZHANG
A11 05  1    @1 TAO WAN
A11 06  1    @1 NAN LI
A11 07  1    @1 XIANGYANG ZHOU
A11 08  1    @1 YANFENG WU
A11 09  1    @1 FENG YANG
A11 10  1    @1 YIZHI YU
A11 11  1    @1 XIAONING WANG
A11 12  1    @1 RUIFU YANG
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C01 01    ENG  @0 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.
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C03 07  X  FRE  @0 Système HLA @5 07
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C03 07  X  SPA  @0 Sistema HLA @5 07
C03 08  X  FRE  @0 Antigène histocompatibilité classe I @5 08
C03 08  X  ENG  @0 Class I histocompatibility antigen @5 08
C03 08  X  SPA  @0 Antígeno histocompatibilidad clase I @5 08
C03 09  X  FRE  @0 Locus HLA-A @5 09
C03 09  X  ENG  @0 HLA-A-Locus @5 09 @6 «HLA-A»-Locus
C03 09  X  SPA  @0 Locus HLA-A @5 09
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C03 11  X  FRE  @0 Lymphocyte T @5 11
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C03 17  X  FRE  @0 Protéine SSp-1 @4 INC @5 87
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C07 01  X  SPA  @0 Virosis @2 NM
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Pascal:04-0586081

Le document en format XML

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<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>
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<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>
</inist>
</record>

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   |wiki=    Sante
   |area=    SrasV1
   |flux=    PascalFrancis
   |étape=   Curation
   |type=    RBID
   |clé=     Pascal:04-0586081
   |texte=   Identification of an HLA-A*0201-restricted CD8+ T-cell epitope SSp- 1 of SARS-CoV spike protein
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