Cross-Allele Cytotoxic T Lymphocyte Responses against 2009 Pandemic H1N1 Influenza A Virus among HLA-A24 and HLA-A3 Supertype-Positive Individuals
Identifieur interne : 000428 ( PascalFrancis/Corpus ); précédent : 000427; suivant : 000429Cross-Allele Cytotoxic T Lymphocyte Responses against 2009 Pandemic H1N1 Influenza A Virus among HLA-A24 and HLA-A3 Supertype-Positive Individuals
Auteurs : JUN LIU ; SHIHONG ZHANG ; SHUGUANG TAN ; YONG YI ; BIN WU ; BIN CAO ; FENGCAI ZHU ; CHEN WANG ; HUA WANG ; JIANXUN QI ; George F. GaoSource :
- Journal of virology [ 0022-538X ] ; 2012.
Descripteurs français
- Pascal (Inist)
English descriptors
Abstract
Lack of a universal vaccine against all serotypes of influenza A viruses and recent progress on T cell-related vaccines against influenza A virus illuminate the important role of human leukocyte antigen (HLA)-restricted cytotoxic T lymphocytes (CTLs) in anti-influenza virus immunity. However, the diverse HLA alleles among humans complicate virus-specific cellular immunity research, and elucidation of cross-HLA allele T cell responses to influenza virus specificity requires further detailed work. An ideal CTL epitope-based vaccine would cover a broad spectrum of epitope antigens presented by most, if not all, of the HLAs. Here, we evaluated the 2009 pandemic influenza A (H1N1) virus-specific T cell responses among the HLA-A24+ population using a rationally designed peptide pool during the 2009 pandemic. Unexpectedly, cross-HLA allele T cell responses against the influenza A virus peptides were detected among both HLA-A11+ and HLA-A24+ donors. Furthermore, we found cross-responses in the entire HLA-A3 supertype population (including HLA-A11, -A31, -A33, and -A30). The cross-allele antigenic peptides within the peptide pool were identified and characterized, and the crystal structures of the major histocompatibility complex (MHC)-peptide complexes were determined. The subsequent HLA-A24-defined cross-allele peptides recognized by the HLA-A11+ population were shown to mildly bind to the HLA-A*1101 molecule. Together with the structural models, these results partially explain the cross-allele responses. Our findings elucidate the promiscuity of the cross-allele T cell responses against influenza A viruses and are beneficial for the development of a T cell epitope-based vaccine applied in a broader population.
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Format Inist (serveur)
NO : | PASCAL 13-0027498 INIST |
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ET : | Cross-Allele Cytotoxic T Lymphocyte Responses against 2009 Pandemic H1N1 Influenza A Virus among HLA-A24 and HLA-A3 Supertype-Positive Individuals |
AU : | JUN LIU; SHIHONG ZHANG; SHUGUANG TAN; YONG YI; BIN WU; BIN CAO; FENGCAI ZHU; CHEN WANG; HUA WANG; JIANXUN QI; GAO (George F.) |
AF : | CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences/Beijing/Chine (1 aut., 2 aut., 3 aut., 10 aut., 11 aut.); China-Japan Joint Laboratory of Molecular Immunology and Molecular Microbiology, Institute of Microbiology, Chinese Academy of Sciences/Beijing/Chine (1 aut., 2 aut., 3 aut., 10 aut., 11 aut.); College of Life Sciences, Graduate University, Chinese Academy of Sciences/Beijing/Chine (2 aut., 3 aut., 11 aut.); Hospital 306th of PLA/Beijing/Chine (4 aut.); Jiangsu Provincial Center for Disease Control and Prevention/Nanjing/Chine (5 aut., 7 aut., 9 aut.); Beijing Chao-Yang Hospital, Beijing Institute of Respiratory Medicine, Capital Medical University/Beijing/Chine (6 aut., 8 aut.); Research Network of Immunity and Health (RNIH), Beijing Institutes of Life Science, Chinese Academy of Sciences/Beijing/Chine (11 aut.) |
DT : | Publication en série; Niveau analytique |
SO : | Journal of virology; ISSN 0022-538X; Etats-Unis; Da. 2012; Vol. 86; No. 24; Pp. 13281-13294; Bibl. 83 ref. |
LA : | Anglais |
EA : | Lack of a universal vaccine against all serotypes of influenza A viruses and recent progress on T cell-related vaccines against influenza A virus illuminate the important role of human leukocyte antigen (HLA)-restricted cytotoxic T lymphocytes (CTLs) in anti-influenza virus immunity. However, the diverse HLA alleles among humans complicate virus-specific cellular immunity research, and elucidation of cross-HLA allele T cell responses to influenza virus specificity requires further detailed work. An ideal CTL epitope-based vaccine would cover a broad spectrum of epitope antigens presented by most, if not all, of the HLAs. Here, we evaluated the 2009 pandemic influenza A (H1N1) virus-specific T cell responses among the HLA-A24+ population using a rationally designed peptide pool during the 2009 pandemic. Unexpectedly, cross-HLA allele T cell responses against the influenza A virus peptides were detected among both HLA-A11+ and HLA-A24+ donors. Furthermore, we found cross-responses in the entire HLA-A3 supertype population (including HLA-A11, -A31, -A33, and -A30). The cross-allele antigenic peptides within the peptide pool were identified and characterized, and the crystal structures of the major histocompatibility complex (MHC)-peptide complexes were determined. The subsequent HLA-A24-defined cross-allele peptides recognized by the HLA-A11+ population were shown to mildly bind to the HLA-A*1101 molecule. Together with the structural models, these results partially explain the cross-allele responses. Our findings elucidate the promiscuity of the cross-allele T cell responses against influenza A viruses and are beneficial for the development of a T cell epitope-based vaccine applied in a broader population. |
CC : | 002A05C10 |
FD : | Virus grippal A; Allèle; Cytotoxicité; Lymphocyte T cytotoxique; Lymphocyte T; Système HLA |
FG : | Influenzavirus A; Orthomyxoviridae; Virus |
ED : | Influenza A virus; Allele; Cytotoxicity; Cytotoxic T lymphocyte; T-Lymphocyte; HLA-System |
EG : | Influenzavirus A; Orthomyxoviridae; Virus |
SD : | Influenza A virus; Alelo; Citotoxicidad; Linfocito T citotóxico; Linfocito T; Sistema HLA |
LO : | INIST-13592.354000506222740120 |
ID : | 13-0027498 |
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Pascal:13-0027498Le document en format XML
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Cross-Allele Cytotoxic T Lymphocyte Responses against 2009 Pandemic H1N1 Influenza A Virus among HLA-A24 and HLA-A3 Supertype-Positive Individuals</title>
<author><name sortKey="Jun Liu" sort="Jun Liu" uniqKey="Jun Liu" last="Jun Liu">JUN LIU</name>
<affiliation><inist:fA14 i1="01"><s1>CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences</s1>
<s2>Beijing</s2>
<s3>CHN</s3>
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<author><name sortKey="Shihong Zhang" sort="Shihong Zhang" uniqKey="Shihong Zhang" last="Shihong Zhang">SHIHONG ZHANG</name>
<affiliation><inist:fA14 i1="01"><s1>CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences</s1>
<s2>Beijing</s2>
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<author><name sortKey="Shuguang Tan" sort="Shuguang Tan" uniqKey="Shuguang Tan" last="Shuguang Tan">SHUGUANG TAN</name>
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<s2>Beijing</s2>
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<s2>Beijing</s2>
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<author><name sortKey="Yong Yi" sort="Yong Yi" uniqKey="Yong Yi" last="Yong Yi">YONG YI</name>
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<author><name sortKey="Bin Wu" sort="Bin Wu" uniqKey="Bin Wu" last="Bin Wu">BIN WU</name>
<affiliation><inist:fA14 i1="05"><s1>Jiangsu Provincial Center for Disease Control and Prevention</s1>
<s2>Nanjing</s2>
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<author><name sortKey="Bin Cao" sort="Bin Cao" uniqKey="Bin Cao" last="Bin Cao">BIN CAO</name>
<affiliation><inist:fA14 i1="06"><s1>Beijing Chao-Yang Hospital, Beijing Institute of Respiratory Medicine, Capital Medical University</s1>
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<author><name sortKey="Fengcai Zhu" sort="Fengcai Zhu" uniqKey="Fengcai Zhu" last="Fengcai Zhu">FENGCAI ZHU</name>
<affiliation><inist:fA14 i1="05"><s1>Jiangsu Provincial Center for Disease Control and Prevention</s1>
<s2>Nanjing</s2>
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<author><name sortKey="Chen Wang" sort="Chen Wang" uniqKey="Chen Wang" last="Chen Wang">CHEN WANG</name>
<affiliation><inist:fA14 i1="06"><s1>Beijing Chao-Yang Hospital, Beijing Institute of Respiratory Medicine, Capital Medical University</s1>
<s2>Beijing</s2>
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<author><name sortKey="Hua Wang" sort="Hua Wang" uniqKey="Hua Wang" last="Hua Wang">HUA WANG</name>
<affiliation><inist:fA14 i1="05"><s1>Jiangsu Provincial Center for Disease Control and Prevention</s1>
<s2>Nanjing</s2>
<s3>CHN</s3>
<sZ>5 aut.</sZ>
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<author><name sortKey="Jianxun Qi" sort="Jianxun Qi" uniqKey="Jianxun Qi" last="Jianxun Qi">JIANXUN QI</name>
<affiliation><inist:fA14 i1="01"><s1>CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences</s1>
<s2>Beijing</s2>
<s3>CHN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
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<affiliation><inist:fA14 i1="02"><s1>China-Japan Joint Laboratory of Molecular Immunology and Molecular Microbiology, Institute of Microbiology, Chinese Academy of Sciences</s1>
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<author><name sortKey="Gao, George F" sort="Gao, George F" uniqKey="Gao G" first="George F." last="Gao">George F. Gao</name>
<affiliation><inist:fA14 i1="01"><s1>CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences</s1>
<s2>Beijing</s2>
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<affiliation><inist:fA14 i1="02"><s1>China-Japan Joint Laboratory of Molecular Immunology and Molecular Microbiology, Institute of Microbiology, Chinese Academy of Sciences</s1>
<s2>Beijing</s2>
<s3>CHN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>10 aut.</sZ>
<sZ>11 aut.</sZ>
</inist:fA14>
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<affiliation><inist:fA14 i1="03"><s1>College of Life Sciences, Graduate University, Chinese Academy of Sciences</s1>
<s2>Beijing</s2>
<s3>CHN</s3>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>11 aut.</sZ>
</inist:fA14>
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<affiliation><inist:fA14 i1="07"><s1>Research Network of Immunity and Health (RNIH), Beijing Institutes of Life Science, Chinese Academy of Sciences</s1>
<s2>Beijing</s2>
<s3>CHN</s3>
<sZ>11 aut.</sZ>
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<title level="j" type="abbreviated">J. virol.</title>
<idno type="ISSN">0022-538X</idno>
</seriesStmt>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Allele</term>
<term>Cytotoxic T lymphocyte</term>
<term>Cytotoxicity</term>
<term>HLA-System</term>
<term>Influenza A virus</term>
<term>T-Lymphocyte</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Virus grippal A</term>
<term>Allèle</term>
<term>Cytotoxicité</term>
<term>Lymphocyte T cytotoxique</term>
<term>Lymphocyte T</term>
<term>Système HLA</term>
</keywords>
</textClass>
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<front><div type="abstract" xml:lang="en">Lack of a universal vaccine against all serotypes of influenza A viruses and recent progress on T cell-related vaccines against influenza A virus illuminate the important role of human leukocyte antigen (HLA)-restricted cytotoxic T lymphocytes (CTLs) in anti-influenza virus immunity. However, the diverse HLA alleles among humans complicate virus-specific cellular immunity research, and elucidation of cross-HLA allele T cell responses to influenza virus specificity requires further detailed work. An ideal CTL epitope-based vaccine would cover a broad spectrum of epitope antigens presented by most, if not all, of the HLAs. Here, we evaluated the 2009 pandemic influenza A (H1N1) virus-specific T cell responses among the HLA-A24<sup>+</sup>
population using a rationally designed peptide pool during the 2009 pandemic. Unexpectedly, cross-HLA allele T cell responses against the influenza A virus peptides were detected among both HLA-A11<sup>+</sup>
and HLA-A24<sup>+</sup>
donors. Furthermore, we found cross-responses in the entire HLA-A3 supertype population (including HLA-A11, -A31, -A33, and -A30). The cross-allele antigenic peptides within the peptide pool were identified and characterized, and the crystal structures of the major histocompatibility complex (MHC)-peptide complexes were determined. The subsequent HLA-A24-defined cross-allele peptides recognized by the HLA-A11<sup>+</sup>
population were shown to mildly bind to the HLA-A<sup>*</sup>
1101 molecule. Together with the structural models, these results partially explain the cross-allele responses. Our findings elucidate the promiscuity of the cross-allele T cell responses against influenza A viruses and are beneficial for the development of a T cell epitope-based vaccine applied in a broader population.</div>
</front>
</TEI>
<inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0022-538X</s0>
</fA01>
<fA03 i2="1"><s0>J. virol.</s0>
</fA03>
<fA05><s2>86</s2>
</fA05>
<fA06><s2>24</s2>
</fA06>
<fA08 i1="01" i2="1" l="ENG"><s1>Cross-Allele Cytotoxic T Lymphocyte Responses against 2009 Pandemic H1N1 Influenza A Virus among HLA-A24 and HLA-A3 Supertype-Positive Individuals</s1>
</fA08>
<fA11 i1="01" i2="1"><s1>JUN LIU</s1>
</fA11>
<fA11 i1="02" i2="1"><s1>SHIHONG ZHANG</s1>
</fA11>
<fA11 i1="03" i2="1"><s1>SHUGUANG TAN</s1>
</fA11>
<fA11 i1="04" i2="1"><s1>YONG YI</s1>
</fA11>
<fA11 i1="05" i2="1"><s1>BIN WU</s1>
</fA11>
<fA11 i1="06" i2="1"><s1>BIN CAO</s1>
</fA11>
<fA11 i1="07" i2="1"><s1>FENGCAI ZHU</s1>
</fA11>
<fA11 i1="08" i2="1"><s1>CHEN WANG</s1>
</fA11>
<fA11 i1="09" i2="1"><s1>HUA WANG</s1>
</fA11>
<fA11 i1="10" i2="1"><s1>JIANXUN QI</s1>
</fA11>
<fA11 i1="11" i2="1"><s1>GAO (George F.)</s1>
</fA11>
<fA14 i1="01"><s1>CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences</s1>
<s2>Beijing</s2>
<s3>CHN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>10 aut.</sZ>
<sZ>11 aut.</sZ>
</fA14>
<fA14 i1="02"><s1>China-Japan Joint Laboratory of Molecular Immunology and Molecular Microbiology, Institute of Microbiology, Chinese Academy of Sciences</s1>
<s2>Beijing</s2>
<s3>CHN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>10 aut.</sZ>
<sZ>11 aut.</sZ>
</fA14>
<fA14 i1="03"><s1>College of Life Sciences, Graduate University, Chinese Academy of Sciences</s1>
<s2>Beijing</s2>
<s3>CHN</s3>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>11 aut.</sZ>
</fA14>
<fA14 i1="04"><s1>Hospital 306th of PLA</s1>
<s2>Beijing</s2>
<s3>CHN</s3>
<sZ>4 aut.</sZ>
</fA14>
<fA14 i1="05"><s1>Jiangsu Provincial Center for Disease Control and Prevention</s1>
<s2>Nanjing</s2>
<s3>CHN</s3>
<sZ>5 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>9 aut.</sZ>
</fA14>
<fA14 i1="06"><s1>Beijing Chao-Yang Hospital, Beijing Institute of Respiratory Medicine, Capital Medical University</s1>
<s2>Beijing</s2>
<s3>CHN</s3>
<sZ>6 aut.</sZ>
<sZ>8 aut.</sZ>
</fA14>
<fA14 i1="07"><s1>Research Network of Immunity and Health (RNIH), Beijing Institutes of Life Science, Chinese Academy of Sciences</s1>
<s2>Beijing</s2>
<s3>CHN</s3>
<sZ>11 aut.</sZ>
</fA14>
<fA20><s1>13281-13294</s1>
</fA20>
<fA21><s1>2012</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
</fA23>
<fA43 i1="01"><s1>INIST</s1>
<s2>13592</s2>
<s5>354000506222740120</s5>
</fA43>
<fA44><s0>0000</s0>
<s1>© 2013 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45><s0>83 ref.</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>13-0027498</s0>
</fA47>
<fA60><s1>P</s1>
</fA60>
<fA61><s0>A</s0>
</fA61>
<fA64 i1="01" i2="1"><s0>Journal of virology</s0>
</fA64>
<fA66 i1="01"><s0>USA</s0>
</fA66>
<fC01 i1="01" l="ENG"><s0>Lack of a universal vaccine against all serotypes of influenza A viruses and recent progress on T cell-related vaccines against influenza A virus illuminate the important role of human leukocyte antigen (HLA)-restricted cytotoxic T lymphocytes (CTLs) in anti-influenza virus immunity. However, the diverse HLA alleles among humans complicate virus-specific cellular immunity research, and elucidation of cross-HLA allele T cell responses to influenza virus specificity requires further detailed work. An ideal CTL epitope-based vaccine would cover a broad spectrum of epitope antigens presented by most, if not all, of the HLAs. Here, we evaluated the 2009 pandemic influenza A (H1N1) virus-specific T cell responses among the HLA-A24<sup>+</sup>
population using a rationally designed peptide pool during the 2009 pandemic. Unexpectedly, cross-HLA allele T cell responses against the influenza A virus peptides were detected among both HLA-A11<sup>+</sup>
and HLA-A24<sup>+</sup>
donors. Furthermore, we found cross-responses in the entire HLA-A3 supertype population (including HLA-A11, -A31, -A33, and -A30). The cross-allele antigenic peptides within the peptide pool were identified and characterized, and the crystal structures of the major histocompatibility complex (MHC)-peptide complexes were determined. The subsequent HLA-A24-defined cross-allele peptides recognized by the HLA-A11<sup>+</sup>
population were shown to mildly bind to the HLA-A<sup>*</sup>
1101 molecule. Together with the structural models, these results partially explain the cross-allele responses. Our findings elucidate the promiscuity of the cross-allele T cell responses against influenza A viruses and are beneficial for the development of a T cell epitope-based vaccine applied in a broader population.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002A05C10</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Virus grippal A</s0>
<s2>NW</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Influenza A virus</s0>
<s2>NW</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Influenza A virus</s0>
<s2>NW</s2>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Allèle</s0>
<s5>05</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Allele</s0>
<s5>05</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Alelo</s0>
<s5>05</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Cytotoxicité</s0>
<s5>06</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Cytotoxicity</s0>
<s5>06</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Citotoxicidad</s0>
<s5>06</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Lymphocyte T cytotoxique</s0>
<s5>07</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Cytotoxic T lymphocyte</s0>
<s5>07</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Linfocito T citotóxico</s0>
<s5>07</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Lymphocyte T</s0>
<s5>08</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>T-Lymphocyte</s0>
<s5>08</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Linfocito T</s0>
<s5>08</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Système HLA</s0>
<s5>09</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>HLA-System</s0>
<s5>09</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Sistema HLA</s0>
<s5>09</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Influenzavirus A</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Influenzavirus A</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Influenzavirus A</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Orthomyxoviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Orthomyxoviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Orthomyxoviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fN21><s1>014</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
</standard>
<server><NO>PASCAL 13-0027498 INIST</NO>
<ET>Cross-Allele Cytotoxic T Lymphocyte Responses against 2009 Pandemic H1N1 Influenza A Virus among HLA-A24 and HLA-A3 Supertype-Positive Individuals</ET>
<AU>JUN LIU; SHIHONG ZHANG; SHUGUANG TAN; YONG YI; BIN WU; BIN CAO; FENGCAI ZHU; CHEN WANG; HUA WANG; JIANXUN QI; GAO (George F.)</AU>
<AF>CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences/Beijing/Chine (1 aut., 2 aut., 3 aut., 10 aut., 11 aut.); China-Japan Joint Laboratory of Molecular Immunology and Molecular Microbiology, Institute of Microbiology, Chinese Academy of Sciences/Beijing/Chine (1 aut., 2 aut., 3 aut., 10 aut., 11 aut.); College of Life Sciences, Graduate University, Chinese Academy of Sciences/Beijing/Chine (2 aut., 3 aut., 11 aut.); Hospital 306th of PLA/Beijing/Chine (4 aut.); Jiangsu Provincial Center for Disease Control and Prevention/Nanjing/Chine (5 aut., 7 aut., 9 aut.); Beijing Chao-Yang Hospital, Beijing Institute of Respiratory Medicine, Capital Medical University/Beijing/Chine (6 aut., 8 aut.); Research Network of Immunity and Health (RNIH), Beijing Institutes of Life Science, Chinese Academy of Sciences/Beijing/Chine (11 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Journal of virology; ISSN 0022-538X; Etats-Unis; Da. 2012; Vol. 86; No. 24; Pp. 13281-13294; Bibl. 83 ref.</SO>
<LA>Anglais</LA>
<EA>Lack of a universal vaccine against all serotypes of influenza A viruses and recent progress on T cell-related vaccines against influenza A virus illuminate the important role of human leukocyte antigen (HLA)-restricted cytotoxic T lymphocytes (CTLs) in anti-influenza virus immunity. However, the diverse HLA alleles among humans complicate virus-specific cellular immunity research, and elucidation of cross-HLA allele T cell responses to influenza virus specificity requires further detailed work. An ideal CTL epitope-based vaccine would cover a broad spectrum of epitope antigens presented by most, if not all, of the HLAs. Here, we evaluated the 2009 pandemic influenza A (H1N1) virus-specific T cell responses among the HLA-A24<sup>+</sup>
population using a rationally designed peptide pool during the 2009 pandemic. Unexpectedly, cross-HLA allele T cell responses against the influenza A virus peptides were detected among both HLA-A11<sup>+</sup>
and HLA-A24<sup>+</sup>
donors. Furthermore, we found cross-responses in the entire HLA-A3 supertype population (including HLA-A11, -A31, -A33, and -A30). The cross-allele antigenic peptides within the peptide pool were identified and characterized, and the crystal structures of the major histocompatibility complex (MHC)-peptide complexes were determined. The subsequent HLA-A24-defined cross-allele peptides recognized by the HLA-A11<sup>+</sup>
population were shown to mildly bind to the HLA-A<sup>*</sup>
1101 molecule. Together with the structural models, these results partially explain the cross-allele responses. Our findings elucidate the promiscuity of the cross-allele T cell responses against influenza A viruses and are beneficial for the development of a T cell epitope-based vaccine applied in a broader population.</EA>
<CC>002A05C10</CC>
<FD>Virus grippal A; Allèle; Cytotoxicité; Lymphocyte T cytotoxique; Lymphocyte T; Système HLA</FD>
<FG>Influenzavirus A; Orthomyxoviridae; Virus</FG>
<ED>Influenza A virus; Allele; Cytotoxicity; Cytotoxic T lymphocyte; T-Lymphocyte; HLA-System</ED>
<EG>Influenzavirus A; Orthomyxoviridae; Virus</EG>
<SD>Influenza A virus; Alelo; Citotoxicidad; Linfocito T citotóxico; Linfocito T; Sistema HLA</SD>
<LO>INIST-13592.354000506222740120</LO>
<ID>13-0027498</ID>
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