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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<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>
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<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>
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<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>
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