Epitope-specific human influenza antibody repertoires diversify by B cell intraclonal sequence divergence and interclonal convergence1
Identifieur interne : 000581 ( Pmc/Corpus ); précédent : 000580; suivant : 000582Epitope-specific human influenza antibody repertoires diversify by B cell intraclonal sequence divergence and interclonal convergence1
Auteurs : Jens C. Krause ; Tshidi Tsibane ; Terrence M. Tumpey ; Chelsey J. Huffman ; Bryan S. Briney ; Scott A. Smith ; Christopher F. Basler ; James E. CroweSource :
- Journal of immunology (Baltimore, Md. : 1950) [ 0022-1767 ] ; 2011.
Abstract
We generated from a single blood sample five independent human monoclonal antibodies that recognized the Sa antigenic site on the head of influenza HA and exhibited inhibitory activity against a broad panel of H1N1 strains. All five Abs used the VH3-7 and JH6 gene segments, but at least four independent clones were identified by junctional analysis. High throughput sequence analysis of circulating B cells revealed that each of the independent clones were members of complex phylogenetic lineages that had diversified widely using a pattern of progressive diversification through somatic mutation. Unexpectedly, B cells encoding multiple diverging lineages of these clones, including many containing very few mutations in the antibody genes, persisted in the circulation. Conversely, we noted frequent instances of amino acid sequence convergence in the antigen combining sites exhibited by members of independent clones, suggesting a strong selection for optimal binding sites. We suggest that maintenance in circulation of a wide diversity of somatic variants of dominant clones may facilitate recognition of drift variant virus epitopes that occur in rapidly mutating virus antigens, such as influenza HA. In fact, these Ab clones recognize an epitope that acquired three glycosylation sites mediating escape from previously isolated human antibodies.
Url:
DOI: 10.4049/jimmunol.1101823
PubMed: 21880983
PubMed Central: 3178754
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PMC:3178754Le document en format XML
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<author><name sortKey="Krause, Jens C" sort="Krause, Jens C" uniqKey="Krause J" first="Jens C." last="Krause">Jens C. Krause</name>
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<author><name sortKey="Tsibane, Tshidi" sort="Tsibane, Tshidi" uniqKey="Tsibane T" first="Tshidi" last="Tsibane">Tshidi Tsibane</name>
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<author><name sortKey="Tumpey, Terrence M" sort="Tumpey, Terrence M" uniqKey="Tumpey T" first="Terrence M." last="Tumpey">Terrence M. Tumpey</name>
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<author><name sortKey="Basler, Christopher F" sort="Basler, Christopher F" uniqKey="Basler C" first="Christopher F." last="Basler">Christopher F. Basler</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Epitope-specific human influenza antibody repertoires diversify by B cell intraclonal sequence divergence and interclonal convergence<sup><xref rid="FN2" ref-type="fn">1</xref>
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<author><name sortKey="Krause, Jens C" sort="Krause, Jens C" uniqKey="Krause J" first="Jens C." last="Krause">Jens C. Krause</name>
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<affiliation><nlm:aff id="A4">Department of Microbiology, Mount Sinai School of Medicine, New York City, NY 10029</nlm:aff>
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<author><name sortKey="Tumpey, Terrence M" sort="Tumpey, Terrence M" uniqKey="Tumpey T" first="Terrence M." last="Tumpey">Terrence M. Tumpey</name>
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<author><name sortKey="Huffman, Chelsey J" sort="Huffman, Chelsey J" uniqKey="Huffman C" first="Chelsey J." last="Huffman">Chelsey J. Huffman</name>
<affiliation><nlm:aff id="A1">Department of Pediatrics, Vanderbilt University Medical Center, Nashville, TN 37232</nlm:aff>
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<author><name sortKey="Briney, Bryan S" sort="Briney, Bryan S" uniqKey="Briney B" first="Bryan S." last="Briney">Bryan S. Briney</name>
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<affiliation><nlm:aff id="A2">Department of Medicine, Vanderbilt University Medical Center, Nashville, TN 37232</nlm:aff>
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<affiliation><nlm:aff id="A1">Department of Pediatrics, Vanderbilt University Medical Center, Nashville, TN 37232</nlm:aff>
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<affiliation><nlm:aff id="A3">Department of Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, TN 37232</nlm:aff>
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<idno type="ISSN">0022-1767</idno>
<idno type="eISSN">1550-6606</idno>
<imprint><date when="2011">2011</date>
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<front><div type="abstract" xml:lang="en"><p id="P1">We generated from a single blood sample five independent human monoclonal antibodies that recognized the Sa antigenic site on the head of influenza HA and exhibited inhibitory activity against a broad panel of H1N1 strains. All five Abs used the V<sub>H</sub>
3-7 and J<sub>H</sub>
6 gene segments, but at least four independent clones were identified by junctional analysis. High throughput sequence analysis of circulating B cells revealed that each of the independent clones were members of complex phylogenetic lineages that had diversified widely using a pattern of progressive diversification through somatic mutation. Unexpectedly, B cells encoding multiple diverging lineages of these clones, including many containing very few mutations in the antibody genes, persisted in the circulation. Conversely, we noted frequent instances of amino acid sequence convergence in the antigen combining sites exhibited by members of independent clones, suggesting a strong selection for optimal binding sites. We suggest that maintenance in circulation of a wide diversity of somatic variants of dominant clones may facilitate recognition of drift variant virus epitopes that occur in rapidly mutating virus antigens, such as influenza HA. In fact, these Ab clones recognize an epitope that acquired three glycosylation sites mediating escape from previously isolated human antibodies.</p>
</div>
</front>
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<front><journal-meta><journal-id journal-id-type="nlm-journal-id">2985117R</journal-id>
<journal-id journal-id-type="pubmed-jr-id">4816</journal-id>
<journal-id journal-id-type="nlm-ta">J Immunol</journal-id>
<journal-title-group><journal-title>Journal of immunology (Baltimore, Md. : 1950)</journal-title>
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<article-categories><subj-group subj-group-type="heading"><subject>Article</subject>
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<title-group><article-title>Epitope-specific human influenza antibody repertoires diversify by B cell intraclonal sequence divergence and interclonal convergence<sup><xref rid="FN2" ref-type="fn">1</xref>
</sup>
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<contrib-group><contrib contrib-type="author"><name><surname>Krause</surname>
<given-names>Jens C.</given-names>
</name>
<xref rid="A1" ref-type="aff">*</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Tsibane</surname>
<given-names>Tshidi</given-names>
</name>
<xref rid="A4" ref-type="aff">§</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Tumpey</surname>
<given-names>Terrence M.</given-names>
</name>
<xref rid="A5" ref-type="aff">¶</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Huffman</surname>
<given-names>Chelsey J.</given-names>
</name>
<xref rid="A1" ref-type="aff">*</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Briney</surname>
<given-names>Bryan S.</given-names>
</name>
<xref rid="A1" ref-type="aff">*</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Smith</surname>
<given-names>Scott A.</given-names>
</name>
<xref rid="A2" ref-type="aff">†</xref>
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<contrib contrib-type="author"><name><surname>Basler</surname>
<given-names>Christopher F.</given-names>
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<xref rid="A4" ref-type="aff">§</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Crowe</surname>
<given-names>James E.</given-names>
<suffix>Jr.</suffix>
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<xref rid="A1" ref-type="aff">*</xref>
<xref rid="A3" ref-type="aff">‡</xref>
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<aff id="A1"><label>*</label>
Department of Pediatrics, Vanderbilt University Medical Center, Nashville, TN 37232</aff>
<aff id="A2"><label>†</label>
Department of Medicine, Vanderbilt University Medical Center, Nashville, TN 37232</aff>
<aff id="A3"><label>‡</label>
Department of Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, TN 37232</aff>
<aff id="A4"><label>§</label>
Department of Microbiology, Mount Sinai School of Medicine, New York City, NY 10029</aff>
<aff id="A5"><label>¶</label>
Influenza Division, Centers for Disease Control and Prevention, Atlanta, GA 30333</aff>
<author-notes><corresp id="FN1">Address correspondence to Dr. James E. Crowe, Jr., Vanderbilt Vaccine Center, Vanderbilt University Medical Center, T-2220 Medical Center North, 1161 21st Avenue South, Nashville, TN 37232-2905., address: <email>james.crowe@vanderbilt.edu</email>
. Telephone: (615) 343-8064. Fax: (615) 343-4456</corresp>
</author-notes>
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<abstract><p id="P1">We generated from a single blood sample five independent human monoclonal antibodies that recognized the Sa antigenic site on the head of influenza HA and exhibited inhibitory activity against a broad panel of H1N1 strains. All five Abs used the V<sub>H</sub>
3-7 and J<sub>H</sub>
6 gene segments, but at least four independent clones were identified by junctional analysis. High throughput sequence analysis of circulating B cells revealed that each of the independent clones were members of complex phylogenetic lineages that had diversified widely using a pattern of progressive diversification through somatic mutation. Unexpectedly, B cells encoding multiple diverging lineages of these clones, including many containing very few mutations in the antibody genes, persisted in the circulation. Conversely, we noted frequent instances of amino acid sequence convergence in the antigen combining sites exhibited by members of independent clones, suggesting a strong selection for optimal binding sites. We suggest that maintenance in circulation of a wide diversity of somatic variants of dominant clones may facilitate recognition of drift variant virus epitopes that occur in rapidly mutating virus antigens, such as influenza HA. In fact, these Ab clones recognize an epitope that acquired three glycosylation sites mediating escape from previously isolated human antibodies.</p>
</abstract>
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