CD93 is required for maintenance of antibody secretion and persistence of plasma cells in the bone marrow niche
Identifieur interne : 001981 ( Pmc/Curation ); précédent : 001980; suivant : 001982CD93 is required for maintenance of antibody secretion and persistence of plasma cells in the bone marrow niche
Auteurs : Stéphane Chevrier [Suisse] ; Céline Genton [Suisse] ; Axel Kallies [Australie] ; Alexander Karnowski [Australie] ; Luc A. Otten [Suisse] ; Bernard Malissen [France] ; Marie Malissen [France] ; Marina Botto [Royaume-Uni] ; Lynn M. Corcoran [Australie] ; Stephen L. Nutt [Australie] ; Hans Acha-Orbea [Suisse]Source :
- Proceedings of the National Academy of Sciences of the United States of America [ 0027-8424 ] ; 2009.
Abstract
Plasma cells represent the end stage of B-cell development and play a key role in providing an efficient antibody response, but they are also involved in numerous pathologies. Here we show that CD93, a receptor expressed during early B-cell development, is reinduced during plasma-cell differentiation. High CD93/CD138 expression was restricted to antibody-secreting cells both in T-dependent and T-independent responses as naive, memory, and germinal-center B cells remained CD93-negative. CD93 was expressed on (pre)plasmablasts/plasma cells, including long-lived plasma cells that showed decreased cell cycle activity, high levels of isotype-switched Ig secretion, and modification of the transcriptional network. T-independent and T-dependent stimuli led to re-expression of CD93 via 2 pathways, either before or after CD138 or Blimp-1 expression. Strikingly, while humoral immune responses initially proceeded normally, CD93-deficient mice were unable to maintain antibody secretion and bone-marrow plasma-cell numbers, demonstrating that CD93 is important for the maintenance of plasma cells in bone marrow niches.
Url:
DOI: 10.1073/pnas.0809736106
PubMed: 19228948
PubMed Central: 2656176
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Otten</name><affiliation wicri:level="1"><nlm:aff id="aff1">Department of Biochemistry, University of Lausanne, Chemin des Boveresses 155, 1066 Epalinges, Switzerland;</nlm:aff><country xml:lang="fr">Suisse</country><wicri:regionArea>Department of Biochemistry, University of Lausanne, Chemin des Boveresses 155, 1066 Epalinges</wicri:regionArea></affiliation></author><author><name sortKey="Malissen, Bernard" sort="Malissen, Bernard" uniqKey="Malissen B" first="Bernard" last="Malissen">Bernard Malissen</name><affiliation wicri:level="1"><nlm:aff wicri:cut="; and" id="aff3">Centre d'Immunologie de Marseille-Luminy, Institut National de la Santé et de la Recherche Médicale/Centre National de la Recherche Scientifique, Université de la Méditerranée, 13284 Marseille, France</nlm:aff><country xml:lang="fr">France</country><wicri:regionArea>Centre d'Immunologie de Marseille-Luminy, Institut National de la Santé et de la Recherche Médicale/Centre National de la Recherche Scientifique, Université de la Méditerranée, 13284 Marseille</wicri:regionArea></affiliation></author><author><name sortKey="Malissen, Marie" sort="Malissen, Marie" uniqKey="Malissen M" first="Marie" last="Malissen">Marie Malissen</name><affiliation wicri:level="1"><nlm:aff wicri:cut="; and" id="aff3">Centre d'Immunologie de Marseille-Luminy, Institut National de la Santé et de la Recherche Médicale/Centre National de la Recherche Scientifique, Université de la Méditerranée, 13284 Marseille, France</nlm:aff><country xml:lang="fr">France</country><wicri:regionArea>Centre d'Immunologie de Marseille-Luminy, Institut National de la Santé et de la Recherche Médicale/Centre National de la Recherche Scientifique, Université de la Méditerranée, 13284 Marseille</wicri:regionArea></affiliation></author><author><name sortKey="Botto, Marina" sort="Botto, Marina" uniqKey="Botto M" first="Marina" last="Botto">Marina Botto</name><affiliation wicri:level="1"><nlm:aff id="aff4">Molecular Genetics and Rheumatology Section, Division of Medicine, Faculty of Medicine, Imperial College, Hammersmith Campus, London W12 0NN, United Kingdom</nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Molecular Genetics and Rheumatology Section, Division of Medicine, Faculty of Medicine, Imperial College, Hammersmith Campus, London W12 0NN</wicri:regionArea></affiliation></author><author><name sortKey="Corcoran, Lynn M" sort="Corcoran, Lynn M" uniqKey="Corcoran L" first="Lynn M." last="Corcoran">Lynn M. Corcoran</name><affiliation wicri:level="1"><nlm:aff id="aff2">The Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, Parkville, Victoria 3050, Australia;</nlm:aff><country xml:lang="fr">Australie</country><wicri:regionArea>The Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, Parkville, Victoria 3050</wicri:regionArea></affiliation></author><author><name sortKey="Nutt, Stephen L" sort="Nutt, Stephen L" uniqKey="Nutt S" first="Stephen L." last="Nutt">Stephen L. Nutt</name><affiliation wicri:level="1"><nlm:aff id="aff2">The Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, Parkville, Victoria 3050, Australia;</nlm:aff><country xml:lang="fr">Australie</country><wicri:regionArea>The Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, Parkville, Victoria 3050</wicri:regionArea></affiliation></author><author><name sortKey="Acha Orbea, Hans" sort="Acha Orbea, Hans" uniqKey="Acha Orbea H" first="Hans" last="Acha-Orbea">Hans Acha-Orbea</name><affiliation wicri:level="1"><nlm:aff id="aff1">Department of Biochemistry, University of Lausanne, Chemin des Boveresses 155, 1066 Epalinges, Switzerland;</nlm:aff><country xml:lang="fr">Suisse</country><wicri:regionArea>Department of Biochemistry, University of Lausanne, Chemin des Boveresses 155, 1066 Epalinges</wicri:regionArea></affiliation></author></analytic><series><title level="j">Proceedings of the National Academy of Sciences of the United States of America</title><idno type="ISSN">0027-8424</idno><idno type="eISSN">1091-6490</idno><imprint><date when="2009">2009</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Plasma cells represent the end stage of B-cell development and play a key role in providing an efficient antibody response, but they are also involved in numerous pathologies. Here we show that CD93, a receptor expressed during early B-cell development, is reinduced during plasma-cell differentiation. High CD93/CD138 expression was restricted to antibody-secreting cells both in T-dependent and T-independent responses as naive, memory, and germinal-center B cells remained CD93-negative. CD93 was expressed on (pre)plasmablasts/plasma cells, including long-lived plasma cells that showed decreased cell cycle activity, high levels of isotype-switched Ig secretion, and modification of the transcriptional network. T-independent and T-dependent stimuli led to re-expression of CD93 via 2 pathways, either before or after CD138 or Blimp-1 expression. Strikingly, while humoral immune responses initially proceeded normally, CD93-deficient mice were unable to maintain antibody secretion and bone-marrow plasma-cell numbers, demonstrating that CD93 is important for the maintenance of plasma cells in bone marrow niches.</p></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Proc Natl Acad Sci U S A</journal-id><journal-id journal-id-type="hwp">pnas</journal-id><journal-id journal-id-type="pmc">pnas</journal-id><journal-id journal-id-type="publisher-id">PNAS</journal-id><journal-title-group><journal-title>Proceedings of the National Academy of Sciences of the United States of America</journal-title></journal-title-group><issn pub-type="ppub">0027-8424</issn><issn pub-type="epub">1091-6490</issn><publisher><publisher-name>National Academy of Sciences</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">19228948</article-id><article-id pub-id-type="pmc">2656176</article-id><article-id pub-id-type="publisher-id">7045</article-id><article-id pub-id-type="doi">10.1073/pnas.0809736106</article-id><article-categories><subj-group subj-group-type="heading"><subject>Biological Sciences</subject><subj-group><subject>Immunology</subject></subj-group></subj-group></article-categories><title-group><article-title>CD93 is required for maintenance of antibody secretion and persistence of plasma cells in the bone marrow niche</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Chevrier</surname><given-names>Stéphane</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref><xref ref-type="author-notes" rid="FN1"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Genton</surname><given-names>Céline</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref><xref ref-type="author-notes" rid="FN1"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Kallies</surname><given-names>Axel</given-names></name><xref ref-type="aff" rid="aff2"><sup>b</sup></xref></contrib><contrib contrib-type="author"><name><surname>Karnowski</surname><given-names>Alexander</given-names></name><xref ref-type="aff" rid="aff2"><sup>b</sup></xref></contrib><contrib contrib-type="author"><name><surname>Otten</surname><given-names>Luc A.</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref></contrib><contrib contrib-type="author"><name><surname>Malissen</surname><given-names>Bernard</given-names></name><xref ref-type="aff" rid="aff3"><sup>c</sup></xref></contrib><contrib contrib-type="author"><name><surname>Malissen</surname><given-names>Marie</given-names></name><xref ref-type="aff" rid="aff3"><sup>c</sup></xref></contrib><contrib contrib-type="author"><name><surname>Botto</surname><given-names>Marina</given-names></name><xref ref-type="aff" rid="aff4"><sup>d</sup></xref></contrib><contrib contrib-type="author"><name><surname>Corcoran</surname><given-names>Lynn M.</given-names></name><xref ref-type="aff" rid="aff2"><sup>b</sup></xref></contrib><contrib contrib-type="author"><name><surname>Nutt</surname><given-names>Stephen L.</given-names></name><xref ref-type="aff" rid="aff2"><sup>b</sup></xref></contrib><contrib contrib-type="author"><name><surname>Acha-Orbea</surname><given-names>Hans</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref><xref ref-type="corresp" rid="cor1"><sup>2</sup></xref></contrib><aff id="aff1"><sup>a</sup>Department of Biochemistry, University of Lausanne, Chemin des Boveresses 155, 1066 Epalinges, Switzerland;</aff><aff id="aff2"><sup>b</sup>The Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, Parkville, Victoria 3050, Australia;</aff><aff id="aff3"><sup>c</sup>Centre d'Immunologie de Marseille-Luminy, Institut National de la Santé et de la Recherche Médicale/Centre National de la Recherche Scientifique, Université de la Méditerranée, 13284 Marseille, France; and</aff><aff id="aff4"><sup>d</sup>Molecular Genetics and Rheumatology Section, Division of Medicine, Faculty of Medicine, Imperial College, Hammersmith Campus, London W12 0NN, United Kingdom</aff></contrib-group><author-notes><corresp id="cor1"><sup>2</sup>To whom correspondence should be addressed. E-mail: <email>hans.acha-orbea@unil.ch</email></corresp><fn fn-type="edited-by"><p>Edited by Gustav J. Nossal, University of Melbourne, Victoria, Australia, and approved January 16, 2009</p></fn><fn fn-type="con"><p>Author contributions: S.C., L.A.O., and H.A.-O. designed research; S.C., C.G., A. Kallies, and A. Karnowski performed research; B.M., M.M., M.B., L.M.C., and S.L.N. contributed new reagents/analytic tools; S.C., C.G., A. Kallies, and A. Karnowski analyzed data; and S.C., A. Kallies, L.M.C., S.L.N., and H.A.-O. wrote the paper.</p></fn><fn fn-type="equal" id="FN1"><p><sup>1</sup>S.C. and C.G. contributed equally to this work.</p></fn></author-notes><pub-date pub-type="ppub"><day>10</day><month>3</month><year>2009</year></pub-date><pub-date pub-type="epub"><day>19</day><month>2</month><year>2009</year></pub-date><volume>106</volume><issue>10</issue><fpage>3895</fpage><lpage>3900</lpage><history><date date-type="received"><day>6</day><month>10</month><year>2008</year></date></history><permissions></permissions><self-uri xlink:title="pdf" xlink:type="simple" xlink:href="zpq01009003895.pdf"></self-uri><abstract><p>Plasma cells represent the end stage of B-cell development and play a key role in providing an efficient antibody response, but they are also involved in numerous pathologies. Here we show that CD93, a receptor expressed during early B-cell development, is reinduced during plasma-cell differentiation. High CD93/CD138 expression was restricted to antibody-secreting cells both in T-dependent and T-independent responses as naive, memory, and germinal-center B cells remained CD93-negative. CD93 was expressed on (pre)plasmablasts/plasma cells, including long-lived plasma cells that showed decreased cell cycle activity, high levels of isotype-switched Ig secretion, and modification of the transcriptional network. T-independent and T-dependent stimuli led to re-expression of CD93 via 2 pathways, either before or after CD138 or Blimp-1 expression. Strikingly, while humoral immune responses initially proceeded normally, CD93-deficient mice were unable to maintain antibody secretion and bone-marrow plasma-cell numbers, demonstrating that CD93 is important for the maintenance of plasma cells in bone marrow niches.</p></abstract><kwd-group><kwd>Aiolos</kwd><kwd>Blimp-1</kwd><kwd>differentiation</kwd><kwd>humoral immunity</kwd><kwd>immunoglobulin</kwd></kwd-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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