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Escape from highly effective public CD8+ T-cell clonotypes by HIV

Identifieur interne : 004601 ( PascalFrancis/Curation ); précédent : 004600; suivant : 004602

Escape from highly effective public CD8+ T-cell clonotypes by HIV

Auteurs : Maria Candela Iglesias [France] ; Jorge R. Almeida [France, États-Unis] ; Solène Fastenackels [France] ; David J. Van Bockel [Australie] ; Masao Hashimoto [Japon] ; Vanessa Venturi [Australie] ; Emma Gostick [Royaume-Uni] ; Alejandra Urrutia [France] ; Linda Wooldridge [Royaume-Uni] ; Mathew Clement [Royaume-Uni] ; Stephanie Gras [Australie] ; Pascal G. Wilmann [Australie] ; Brigitte Autran [France] ; Arnaud Moris [France] ; Jamie Rossjohn [Australie] ; Miles P. Davenport [Australie] ; Masafumi Takiguchi [Japon] ; Christian Brander [Espagne] ; Daniel C. Douek [États-Unis] ; Anthony D. Kelleher [Australie] ; David A. Price [États-Unis, Royaume-Uni] ; Victor Appay [France]

Source :

RBID : Pascal:11-0412237

Descripteurs français

English descriptors

Abstract

Mapping the precise determinants of T-cell efficacy against viruses in humans is a public health priority with crucial implications for vaccine design. To inform this effort, we performed a comprehensive analysis of the effective CD8+ T-cell clonotypes that constitute responses specific for the HIV p24 Gag-derived KK10 epitope (KRWIILGLNK; residues 263-272) restricted by HLA-B*2705, which are known to confer superior control of viral replication in HIV-infected individuals. Particular KK10-specific CD8+ T-cell clonotypes, characterized by TRBV4-3/TRBJ1-3 gene rearrangements, were found to be preferentially selected in vivo and shared between individuals. These "public" clonotypes exhibit high levels of TCR avidity and Ag sensitivity, which impart functional advantages and enable effective suppression of HIV replication. The early L268M mutation at position 6 of the KK10 epitope enables the virus to avoid recognition by these highly effective CD8+ T-cell clonotypes. However, alternative clonotypes with variant reactivity provide flexibility within the overall KK10-specific response. These findings provide refined mechanistic insights into the workings of an effective CD8+ T-cell response against HIV.
pA  
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A08 01  1  ENG  @1 Escape from highly effective public CD8+ T-cell clonotypes by HIV
A11 01  1    @1 CANDELA IGLESIAS (Maria)
A11 02  1    @1 ALMEIDA (Jorge R.)
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A11 12  1    @1 WILMANN (Pascal G.)
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A11 15  1    @1 ROSSJOHN (Jamie)
A11 16  1    @1 DAVENPORT (Miles P.)
A11 17  1    @1 TAKIGUCHI (Masafumi)
A11 18  1    @1 BRANDER (Christian)
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A14 02      @1 Human Immunology Section, Vaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health @2 Bethesda, MD @3 USA @Z 2 aut. @Z 19 aut. @Z 21 aut.
A14 03      @1 St Vincent's Centre for Applied Medical Research and the Kirby Institute, University of New South Wales @2 Darlinghurst @3 AUS @Z 4 aut. @Z 20 aut.
A14 04      @1 Division of Viral Immunology, Center for AIDS Research, Kumamoto University @2 Kumamoto @3 JPN @Z 5 aut. @Z 17 aut.
A14 05      @1 Computational Biology Group, Centre for Vascular Research, University of New South Wales @2 Kensington @3 AUS @Z 6 aut.
A14 06      @1 Department of Infection, Immunity and Biochemistry, Cardiff University School of Medicine @2 Cardiff @3 GBR @Z 7 aut. @Z 9 aut. @Z 10 aut. @Z 21 aut.
A14 07      @1 Department of Biochemistry and Molecular Biology, School of Biomedical Sciences, Monash University @2 Victoria @3 AUS @Z 11 aut. @Z 12 aut. @Z 15 aut.
A14 08      @1 AP-HP, Groupe Hospitalier Pitié-Salpêtrière, Laboratoire d'Immunologie Cellulaire et Tssulaire @2 Paris @3 FRA @Z 13 aut. @Z 22 aut.
A14 09      @1 Complex Systems in Biology Group, Centre for Vascular Research, University of New South Wales @2 Kensington @3 AUS @Z 16 aut.
A14 10      @1 AIDS Research Institute IrsiCaixa-HIVACAT, Hospital Universitari Germans Trias i Pujol Ctra del Canyet @2 Barcelona @3 ESP @Z 18 aut.
A14 11      @1 Institució Catalana de Recerca i Estudis Avançats (ICREA) @2 Barcelona @3 ESP @Z 18 aut.
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C01 01    ENG  @0 Mapping the precise determinants of T-cell efficacy against viruses in humans is a public health priority with crucial implications for vaccine design. To inform this effort, we performed a comprehensive analysis of the effective CD8+ T-cell clonotypes that constitute responses specific for the HIV p24 Gag-derived KK10 epitope (KRWIILGLNK; residues 263-272) restricted by HLA-B*2705, which are known to confer superior control of viral replication in HIV-infected individuals. Particular KK10-specific CD8+ T-cell clonotypes, characterized by TRBV4-3/TRBJ1-3 gene rearrangements, were found to be preferentially selected in vivo and shared between individuals. These "public" clonotypes exhibit high levels of TCR avidity and Ag sensitivity, which impart functional advantages and enable effective suppression of HIV replication. The early L268M mutation at position 6 of the KK10 epitope enables the virus to avoid recognition by these highly effective CD8+ T-cell clonotypes. However, alternative clonotypes with variant reactivity provide flexibility within the overall KK10-specific response. These findings provide refined mechanistic insights into the workings of an effective CD8+ T-cell response against HIV.
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Pascal:11-0412237

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<name sortKey="Urrutia, Alejandra" sort="Urrutia, Alejandra" uniqKey="Urrutia A" first="Alejandra" last="Urrutia">Alejandra Urrutia</name>
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<name sortKey="Wooldridge, Linda" sort="Wooldridge, Linda" uniqKey="Wooldridge L" first="Linda" last="Wooldridge">Linda Wooldridge</name>
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<name sortKey="Clement, Mathew" sort="Clement, Mathew" uniqKey="Clement M" first="Mathew" last="Clement">Mathew Clement</name>
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<name sortKey="Gras, Stephanie" sort="Gras, Stephanie" uniqKey="Gras S" first="Stephanie" last="Gras">Stephanie Gras</name>
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<name sortKey="Autran, Brigitte" sort="Autran, Brigitte" uniqKey="Autran B" first="Brigitte" last="Autran">Brigitte Autran</name>
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<name sortKey="Moris, Arnaud" sort="Moris, Arnaud" uniqKey="Moris A" first="Arnaud" last="Moris">Arnaud Moris</name>
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<name sortKey="Rossjohn, Jamie" sort="Rossjohn, Jamie" uniqKey="Rossjohn J" first="Jamie" last="Rossjohn">Jamie Rossjohn</name>
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<s1>Department of Biochemistry and Molecular Biology, School of Biomedical Sciences, Monash University</s1>
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<name sortKey="Davenport, Miles P" sort="Davenport, Miles P" uniqKey="Davenport M" first="Miles P." last="Davenport">Miles P. Davenport</name>
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<s1>Complex Systems in Biology Group, Centre for Vascular Research, University of New South Wales</s1>
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<author>
<name sortKey="Takiguchi, Masafumi" sort="Takiguchi, Masafumi" uniqKey="Takiguchi M" first="Masafumi" last="Takiguchi">Masafumi Takiguchi</name>
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<s1>Division of Viral Immunology, Center for AIDS Research, Kumamoto University</s1>
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<name sortKey="Brander, Christian" sort="Brander, Christian" uniqKey="Brander C" first="Christian" last="Brander">Christian Brander</name>
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<s1>AIDS Research Institute IrsiCaixa-HIVACAT, Hospital Universitari Germans Trias i Pujol Ctra del Canyet</s1>
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<affiliation wicri:level="1">
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<s1>Institució Catalana de Recerca i Estudis Avançats (ICREA)</s1>
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<country>Espagne</country>
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<author>
<name sortKey="Douek, Daniel C" sort="Douek, Daniel C" uniqKey="Douek D" first="Daniel C." last="Douek">Daniel C. Douek</name>
<affiliation wicri:level="1">
<inist:fA14 i1="02">
<s1>Human Immunology Section, Vaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health</s1>
<s2>Bethesda, MD</s2>
<s3>USA</s3>
<sZ>2 aut.</sZ>
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<country>États-Unis</country>
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<author>
<name sortKey="Kelleher, Anthony D" sort="Kelleher, Anthony D" uniqKey="Kelleher A" first="Anthony D." last="Kelleher">Anthony D. Kelleher</name>
<affiliation wicri:level="1">
<inist:fA14 i1="03">
<s1>St Vincent's Centre for Applied Medical Research and the Kirby Institute, University of New South Wales</s1>
<s2>Darlinghurst</s2>
<s3>AUS</s3>
<sZ>4 aut.</sZ>
<sZ>20 aut.</sZ>
</inist:fA14>
<country>Australie</country>
</affiliation>
</author>
<author>
<name sortKey="Price, David A" sort="Price, David A" uniqKey="Price D" first="David A." last="Price">David A. Price</name>
<affiliation wicri:level="1">
<inist:fA14 i1="02">
<s1>Human Immunology Section, Vaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health</s1>
<s2>Bethesda, MD</s2>
<s3>USA</s3>
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<title xml:lang="en" level="a">Escape from highly effective public CD8
<sup>+</sup>
T-cell clonotypes by HIV</title>
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<name sortKey="Candela Iglesias, Maria" sort="Candela Iglesias, Maria" uniqKey="Candela Iglesias M" first="Maria" last="Candela Iglesias">Maria Candela Iglesias</name>
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<author>
<name sortKey="Almeida, Jorge R" sort="Almeida, Jorge R" uniqKey="Almeida J" first="Jorge R." last="Almeida">Jorge R. Almeida</name>
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<name sortKey="Hashimoto, Masao" sort="Hashimoto, Masao" uniqKey="Hashimoto M" first="Masao" last="Hashimoto">Masao Hashimoto</name>
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<name sortKey="Urrutia, Alejandra" sort="Urrutia, Alejandra" uniqKey="Urrutia A" first="Alejandra" last="Urrutia">Alejandra Urrutia</name>
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<name sortKey="Gras, Stephanie" sort="Gras, Stephanie" uniqKey="Gras S" first="Stephanie" last="Gras">Stephanie Gras</name>
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<name sortKey="Moris, Arnaud" sort="Moris, Arnaud" uniqKey="Moris A" first="Arnaud" last="Moris">Arnaud Moris</name>
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<s1>Department of Biochemistry and Molecular Biology, School of Biomedical Sciences, Monash University</s1>
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<s1>Division of Viral Immunology, Center for AIDS Research, Kumamoto University</s1>
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<country>Japon</country>
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<name sortKey="Brander, Christian" sort="Brander, Christian" uniqKey="Brander C" first="Christian" last="Brander">Christian Brander</name>
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<s1>AIDS Research Institute IrsiCaixa-HIVACAT, Hospital Universitari Germans Trias i Pujol Ctra del Canyet</s1>
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<country>Espagne</country>
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<s1>Institució Catalana de Recerca i Estudis Avançats (ICREA)</s1>
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<name sortKey="Kelleher, Anthony D" sort="Kelleher, Anthony D" uniqKey="Kelleher A" first="Anthony D." last="Kelleher">Anthony D. Kelleher</name>
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<name sortKey="Appay, Victor" sort="Appay, Victor" uniqKey="Appay V" first="Victor" last="Appay">Victor Appay</name>
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<series>
<title level="j" type="main">Blood</title>
<title level="j" type="abbreviated">Blood</title>
<idno type="ISSN">0006-4971</idno>
<imprint>
<date when="2011">2011</date>
</imprint>
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<title level="j" type="main">Blood</title>
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<keywords scheme="KwdEn" xml:lang="en">
<term>AIDS</term>
<term>CD8 T lymphocyte</term>
<term>Efficiency</term>
<term>Hematology</term>
<term>Human immunodeficiency virus</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr">
<term>SIDA</term>
<term>Efficacité</term>
<term>Lymphocyte T CD8</term>
<term>Virus immunodéficience humaine</term>
<term>Hématologie</term>
</keywords>
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<front>
<div type="abstract" xml:lang="en">Mapping the precise determinants of T-cell efficacy against viruses in humans is a public health priority with crucial implications for vaccine design. To inform this effort, we performed a comprehensive analysis of the effective CD8
<sup>+</sup>
T-cell clonotypes that constitute responses specific for the HIV p24 Gag-derived KK10 epitope (KRWIILGLNK; residues 263-272) restricted by HLA-B
<sup>*</sup>
2705, which are known to confer superior control of viral replication in HIV-infected individuals. Particular KK10-specific CD8
<sup>+</sup>
T-cell clonotypes, characterized by TRBV4-3/TRBJ1-3 gene rearrangements, were found to be preferentially selected in vivo and shared between individuals. These "public" clonotypes exhibit high levels of TCR avidity and Ag sensitivity, which impart functional advantages and enable effective suppression of HIV replication. The early L
<sub>268</sub>
M mutation at position 6 of the KK10 epitope enables the virus to avoid recognition by these highly effective CD8
<sup>+</sup>
T-cell clonotypes. However, alternative clonotypes with variant reactivity provide flexibility within the overall KK10-specific response. These findings provide refined mechanistic insights into the workings of an effective CD8
<sup>+</sup>
T-cell response against HIV.</div>
</front>
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<s1>PRICE (David A.)</s1>
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<fA11 i1="22" i2="1">
<s1>APPAY (Victor)</s1>
</fA11>
<fA14 i1="01">
<s1>Inserm UMR S 945, Infections and Immunity, Avenir Group, Université Pierre et Marie Curie-Paris 6, Hôpital Pitié-Salpêtrière</s1>
<s2>Paris</s2>
<s3>FRA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>13 aut.</sZ>
<sZ>14 aut.</sZ>
<sZ>22 aut.</sZ>
</fA14>
<fA14 i1="02">
<s1>Human Immunology Section, Vaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health</s1>
<s2>Bethesda, MD</s2>
<s3>USA</s3>
<sZ>2 aut.</sZ>
<sZ>19 aut.</sZ>
<sZ>21 aut.</sZ>
</fA14>
<fA14 i1="03">
<s1>St Vincent's Centre for Applied Medical Research and the Kirby Institute, University of New South Wales</s1>
<s2>Darlinghurst</s2>
<s3>AUS</s3>
<sZ>4 aut.</sZ>
<sZ>20 aut.</sZ>
</fA14>
<fA14 i1="04">
<s1>Division of Viral Immunology, Center for AIDS Research, Kumamoto University</s1>
<s2>Kumamoto</s2>
<s3>JPN</s3>
<sZ>5 aut.</sZ>
<sZ>17 aut.</sZ>
</fA14>
<fA14 i1="05">
<s1>Computational Biology Group, Centre for Vascular Research, University of New South Wales</s1>
<s2>Kensington</s2>
<s3>AUS</s3>
<sZ>6 aut.</sZ>
</fA14>
<fA14 i1="06">
<s1>Department of Infection, Immunity and Biochemistry, Cardiff University School of Medicine</s1>
<s2>Cardiff</s2>
<s3>GBR</s3>
<sZ>7 aut.</sZ>
<sZ>9 aut.</sZ>
<sZ>10 aut.</sZ>
<sZ>21 aut.</sZ>
</fA14>
<fA14 i1="07">
<s1>Department of Biochemistry and Molecular Biology, School of Biomedical Sciences, Monash University</s1>
<s2>Victoria</s2>
<s3>AUS</s3>
<sZ>11 aut.</sZ>
<sZ>12 aut.</sZ>
<sZ>15 aut.</sZ>
</fA14>
<fA14 i1="08">
<s1>AP-HP, Groupe Hospitalier Pitié-Salpêtrière, Laboratoire d'Immunologie Cellulaire et Tssulaire</s1>
<s2>Paris</s2>
<s3>FRA</s3>
<sZ>13 aut.</sZ>
<sZ>22 aut.</sZ>
</fA14>
<fA14 i1="09">
<s1>Complex Systems in Biology Group, Centre for Vascular Research, University of New South Wales</s1>
<s2>Kensington</s2>
<s3>AUS</s3>
<sZ>16 aut.</sZ>
</fA14>
<fA14 i1="10">
<s1>AIDS Research Institute IrsiCaixa-HIVACAT, Hospital Universitari Germans Trias i Pujol Ctra del Canyet</s1>
<s2>Barcelona</s2>
<s3>ESP</s3>
<sZ>18 aut.</sZ>
</fA14>
<fA14 i1="11">
<s1>Institució Catalana de Recerca i Estudis Avançats (ICREA)</s1>
<s2>Barcelona</s2>
<s3>ESP</s3>
<sZ>18 aut.</sZ>
</fA14>
<fA20>
<s1>2138-2149</s1>
</fA20>
<fA21>
<s1>2011</s1>
</fA21>
<fA23 i1="01">
<s0>ENG</s0>
</fA23>
<fA43 i1="01">
<s1>INIST</s1>
<s2>3178</s2>
<s5>354000508970090160</s5>
</fA43>
<fA44>
<s0>0000</s0>
<s1>© 2011 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45>
<s0>50 ref.</s0>
</fA45>
<fA47 i1="01" i2="1">
<s0>11-0412237</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>Mapping the precise determinants of T-cell efficacy against viruses in humans is a public health priority with crucial implications for vaccine design. To inform this effort, we performed a comprehensive analysis of the effective CD8
<sup>+</sup>
T-cell clonotypes that constitute responses specific for the HIV p24 Gag-derived KK10 epitope (KRWIILGLNK; residues 263-272) restricted by HLA-B
<sup>*</sup>
2705, which are known to confer superior control of viral replication in HIV-infected individuals. Particular KK10-specific CD8
<sup>+</sup>
T-cell clonotypes, characterized by TRBV4-3/TRBJ1-3 gene rearrangements, were found to be preferentially selected in vivo and shared between individuals. These "public" clonotypes exhibit high levels of TCR avidity and Ag sensitivity, which impart functional advantages and enable effective suppression of HIV replication. The early L
<sub>268</sub>
M mutation at position 6 of the KK10 epitope enables the virus to avoid recognition by these highly effective CD8
<sup>+</sup>
T-cell clonotypes. However, alternative clonotypes with variant reactivity provide flexibility within the overall KK10-specific response. These findings provide refined mechanistic insights into the workings of an effective CD8
<sup>+</sup>
T-cell response against HIV.</s0>
</fC01>
<fC02 i1="01" i2="X">
<s0>002B19</s0>
</fC02>
<fC02 i1="02" i2="X">
<s0>002B05C02D</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE">
<s0>SIDA</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG">
<s0>AIDS</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA">
<s0>SIDA</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE">
<s0>Efficacité</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG">
<s0>Efficiency</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA">
<s0>Eficacia</s0>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE">
<s0>Lymphocyte T CD8</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG">
<s0>CD8 T lymphocyte</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA">
<s0>Linfocito T CD8</s0>
<s5>03</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE">
<s0>Virus immunodéficience humaine</s0>
<s2>NW</s2>
<s5>05</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG">
<s0>Human immunodeficiency virus</s0>
<s2>NW</s2>
<s5>05</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA">
<s0>Human immunodeficiency virus</s0>
<s2>NW</s2>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE">
<s0>Hématologie</s0>
<s5>06</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG">
<s0>Hematology</s0>
<s5>06</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA">
<s0>Hematología</s0>
<s5>06</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE">
<s0>Virose</s0>
</fC07>
<fC07 i1="01" i2="X" l="ENG">
<s0>Viral disease</s0>
</fC07>
<fC07 i1="01" i2="X" l="SPA">
<s0>Virosis</s0>
</fC07>
<fC07 i1="02" i2="X" l="FRE">
<s0>Infection</s0>
</fC07>
<fC07 i1="02" i2="X" l="ENG">
<s0>Infection</s0>
</fC07>
<fC07 i1="02" i2="X" l="SPA">
<s0>Infección</s0>
</fC07>
<fC07 i1="03" i2="X" l="FRE">
<s0>Lentivirus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="ENG">
<s0>Lentivirus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA">
<s0>Lentivirus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="04" i2="X" l="FRE">
<s0>Retroviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="04" i2="X" l="ENG">
<s0>Retroviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="04" i2="X" l="SPA">
<s0>Retroviridae</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>Immunodéficit</s0>
<s5>37</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG">
<s0>Immune deficiency</s0>
<s5>37</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA">
<s0>Inmunodeficiencia</s0>
<s5>37</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE">
<s0>Immunopathologie</s0>
<s5>39</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG">
<s0>Immunopathology</s0>
<s5>39</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA">
<s0>Inmunopatología</s0>
<s5>39</s5>
</fC07>
<fN21>
<s1>283</s1>
</fN21>
<fN44 i1="01">
<s1>OTO</s1>
</fN44>
<fN82>
<s1>OTO</s1>
</fN82>
</pA>
</standard>
</inist>
</record>

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