Immunosurveillance and therapy of multiple myeloma are CD226 dependent
Identifieur interne : 000199 ( Pmc/Corpus ); précédent : 000198; suivant : 000200Immunosurveillance and therapy of multiple myeloma are CD226 dependent
Auteurs : Camille Guillerey ; Lucas Ferrari De Andrade ; Slavica Vuckovic ; Kim Miles ; Shin Foong Ngiow ; Michelle C. R. Yong ; Michele W. L. Teng ; Marco Colonna ; David S. Ritchie ; Martha Chesi ; P. Leif Bergsagel ; Geoffrey R. Hill ; Mark J. Smyth ; Ludovic MartinetSource :
- The Journal of Clinical Investigation [ 0021-9738 ] ; 2015.
Abstract
Multiple myeloma (MM) is an age-dependent hematological malignancy. Evaluation of immune interactions that drive MM relies on in vitro experiments that do not reflect the complex cellular stroma involved in MM pathogenesis. Here we used Vk*MYC transgenic mice, which spontaneously develop MM, and demonstrated that the immune system plays a critical role in the control of MM progression and the response to treatment. We monitored Vk*MYC mice that had been crossed with
Url:
DOI: 10.1172/JCI77181
PubMed: 25893601
PubMed Central: 4463191
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PMC:4463191Le document en format XML
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<author><name sortKey="Guillerey, Camille" sort="Guillerey, Camille" uniqKey="Guillerey C" first="Camille" last="Guillerey">Camille Guillerey</name>
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<author><name sortKey="Colonna, Marco" sort="Colonna, Marco" uniqKey="Colonna M" first="Marco" last="Colonna">Marco Colonna</name>
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<author><name sortKey="Chesi, Martha" sort="Chesi, Martha" uniqKey="Chesi M" first="Martha" last="Chesi">Martha Chesi</name>
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<author><name sortKey="Hill, Geoffrey R" sort="Hill, Geoffrey R" uniqKey="Hill G" first="Geoffrey R." last="Hill">Geoffrey R. Hill</name>
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<author><name sortKey="Smyth, Mark J" sort="Smyth, Mark J" uniqKey="Smyth M" first="Mark J." last="Smyth">Mark J. Smyth</name>
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</affiliation>
<affiliation><nlm:aff id="A2">School of Medicine, University of Queensland, Herston, Queensland, Australia.</nlm:aff>
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<author><name sortKey="Martinet, Ludovic" sort="Martinet, Ludovic" uniqKey="Martinet L" first="Ludovic" last="Martinet">Ludovic Martinet</name>
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<affiliation><nlm:aff id="A9">INSERM UMR 1037, Cancer Research Center of Toulouse, Toulouse, France.</nlm:aff>
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</affiliation>
<affiliation><nlm:aff id="A2">School of Medicine, University of Queensland, Herston, Queensland, Australia.</nlm:aff>
</affiliation>
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<author><name sortKey="Ferrari De Andrade, Lucas" sort="Ferrari De Andrade, Lucas" uniqKey="Ferrari De Andrade L" first="Lucas" last="Ferrari De Andrade">Lucas Ferrari De Andrade</name>
<affiliation><nlm:aff id="A1">Immunology of Cancer and Infection Laboratory, QIMR Berghofer Medical Research Institute, Herston, Queensland, Australia.</nlm:aff>
</affiliation>
<affiliation><nlm:aff id="A3">Células Inflamatórias e Neoplásicas group, Universidade Federal do Paraná, Curitiba, Paraná, Brazil.</nlm:aff>
</affiliation>
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<author><name sortKey="Vuckovic, Slavica" sort="Vuckovic, Slavica" uniqKey="Vuckovic S" first="Slavica" last="Vuckovic">Slavica Vuckovic</name>
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<author><name sortKey="Miles, Kim" sort="Miles, Kim" uniqKey="Miles K" first="Kim" last="Miles">Kim Miles</name>
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</affiliation>
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<author><name sortKey="Ngiow, Shin Foong" sort="Ngiow, Shin Foong" uniqKey="Ngiow S" first="Shin Foong" last="Ngiow">Shin Foong Ngiow</name>
<affiliation><nlm:aff id="A1">Immunology of Cancer and Infection Laboratory, QIMR Berghofer Medical Research Institute, Herston, Queensland, Australia.</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Yong, Michelle C R" sort="Yong, Michelle C R" uniqKey="Yong M" first="Michelle C. R." last="Yong">Michelle C. R. Yong</name>
<affiliation><nlm:aff id="A5">Cancer Immunoregulation and Immunotherapy Laboratory, QIMR Berghofer Medical Research Institute, Herston, Queensland, Australia.</nlm:aff>
</affiliation>
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<author><name sortKey="Teng, Michele W L" sort="Teng, Michele W L" uniqKey="Teng M" first="Michele W. L." last="Teng">Michele W. L. Teng</name>
<affiliation><nlm:aff id="A5">Cancer Immunoregulation and Immunotherapy Laboratory, QIMR Berghofer Medical Research Institute, Herston, Queensland, Australia.</nlm:aff>
</affiliation>
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<author><name sortKey="Colonna, Marco" sort="Colonna, Marco" uniqKey="Colonna M" first="Marco" last="Colonna">Marco Colonna</name>
<affiliation><nlm:aff id="A6">Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, Missouri, USA.</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Ritchie, David S" sort="Ritchie, David S" uniqKey="Ritchie D" first="David S." last="Ritchie">David S. Ritchie</name>
<affiliation><nlm:aff id="A7">Sir Peter MacCallum Department of Oncology, University of Melbourne, Parkville, Victoria, Australia.</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Chesi, Martha" sort="Chesi, Martha" uniqKey="Chesi M" first="Martha" last="Chesi">Martha Chesi</name>
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</affiliation>
</author>
<author><name sortKey="Bergsagel, P Leif" sort="Bergsagel, P Leif" uniqKey="Bergsagel P" first="P. Leif" last="Bergsagel">P. Leif Bergsagel</name>
<affiliation><nlm:aff id="A8">Comprehensive Cancer Center, Mayo Clinic, Scottsdale, Arizona, USA.</nlm:aff>
</affiliation>
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<author><name sortKey="Hill, Geoffrey R" sort="Hill, Geoffrey R" uniqKey="Hill G" first="Geoffrey R." last="Hill">Geoffrey R. Hill</name>
<affiliation><nlm:aff wicri:cut=" and" id="A4">Bone Marrow Transplantation</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Smyth, Mark J" sort="Smyth, Mark J" uniqKey="Smyth M" first="Mark J." last="Smyth">Mark J. Smyth</name>
<affiliation><nlm:aff id="A1">Immunology of Cancer and Infection Laboratory, QIMR Berghofer Medical Research Institute, Herston, Queensland, Australia.</nlm:aff>
</affiliation>
<affiliation><nlm:aff id="A2">School of Medicine, University of Queensland, Herston, Queensland, Australia.</nlm:aff>
</affiliation>
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<author><name sortKey="Martinet, Ludovic" sort="Martinet, Ludovic" uniqKey="Martinet L" first="Ludovic" last="Martinet">Ludovic Martinet</name>
<affiliation><nlm:aff id="A1">Immunology of Cancer and Infection Laboratory, QIMR Berghofer Medical Research Institute, Herston, Queensland, Australia.</nlm:aff>
</affiliation>
<affiliation><nlm:aff id="A9">INSERM UMR 1037, Cancer Research Center of Toulouse, Toulouse, France.</nlm:aff>
</affiliation>
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<series><title level="j">The Journal of Clinical Investigation</title>
<idno type="ISSN">0021-9738</idno>
<idno type="eISSN">1558-8238</idno>
<imprint><date when="2015">2015</date>
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<front><div type="abstract" xml:lang="en"><p>Multiple myeloma (MM) is an age-dependent hematological malignancy. Evaluation of immune interactions that drive MM relies on in vitro experiments that do not reflect the complex cellular stroma involved in MM pathogenesis. Here we used Vk*MYC transgenic mice, which spontaneously develop MM, and demonstrated that the immune system plays a critical role in the control of MM progression and the response to treatment. We monitored Vk*MYC mice that had been crossed with <italic>Cd226</italic>
mutant mice over a period of 3 years and found that CD226 limits spontaneous MM development. The CD226-dependent anti-myeloma immune response against transplanted Vk*MYC MM cells was mediated both by NK and CD8<sup>+</sup>
T cells through perforin and IFN-γ pathways. Moreover, CD226 expression was required for optimal antimyeloma efficacy of cyclophosphamide (CTX) and bortezomib (Btz), which are both standardly used to manage MM in patients. Activation of costimulatory receptor CD137 with mAb (4-1BB) exerted strong antimyeloma activity, while inhibition of coinhibitory receptors PD-1 and CTLA-4 had no effect. Taken together, the results of this study provide in vivo evidence that CD226 is important for MM immunosurveillance and indicate that specific immune components should be targeted for optimal MM treatment efficacy. As progressive immunosuppression associates with MM development, strategies aimed to increase immune functions may have important therapeutic implications in MM.</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">J Clin Invest</journal-id>
<journal-id journal-id-type="iso-abbrev">J. Clin. Invest</journal-id>
<journal-id journal-id-type="publisher-id">J CLIN INVEST</journal-id>
<journal-title-group><journal-title>The Journal of Clinical Investigation</journal-title>
</journal-title-group>
<issn pub-type="ppub">0021-9738</issn>
<issn pub-type="epub">1558-8238</issn>
<publisher><publisher-name>American Society for Clinical Investigation</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">25893601</article-id>
<article-id pub-id-type="pmc">4463191</article-id>
<article-id pub-id-type="publisher-id">77181</article-id>
<article-id pub-id-type="doi">10.1172/JCI77181</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject>
</subj-group>
</article-categories>
<title-group><article-title>Immunosurveillance and therapy of multiple myeloma are CD226 dependent</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Guillerey</surname>
<given-names>Camille</given-names>
</name>
<xref ref-type="aff" rid="A1">1</xref>
<xref ref-type="aff" rid="A2">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Ferrari de Andrade</surname>
<given-names>Lucas</given-names>
</name>
<xref ref-type="aff" rid="A1">1</xref>
<xref ref-type="aff" rid="A3">3</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Vuckovic</surname>
<given-names>Slavica</given-names>
</name>
<xref ref-type="aff" rid="A4">4</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Miles</surname>
<given-names>Kim</given-names>
</name>
<xref ref-type="aff" rid="A1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Ngiow</surname>
<given-names>Shin Foong</given-names>
</name>
<xref ref-type="aff" rid="A1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Yong</surname>
<given-names>Michelle C.R.</given-names>
</name>
<xref ref-type="aff" rid="A5">5</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Teng</surname>
<given-names>Michele W.L.</given-names>
</name>
<xref ref-type="aff" rid="A5">5</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Colonna</surname>
<given-names>Marco</given-names>
</name>
<xref ref-type="aff" rid="A6">6</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Ritchie</surname>
<given-names>David S.</given-names>
</name>
<xref ref-type="aff" rid="A7">7</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Chesi</surname>
<given-names>Martha</given-names>
</name>
<xref ref-type="aff" rid="A8">8</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Bergsagel</surname>
<given-names>P. Leif</given-names>
</name>
<xref ref-type="aff" rid="A8">8</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Hill</surname>
<given-names>Geoffrey R.</given-names>
</name>
<xref ref-type="aff" rid="A4">4</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Smyth</surname>
<given-names>Mark J.</given-names>
</name>
<xref ref-type="aff" rid="A1">1</xref>
<xref ref-type="aff" rid="A2">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Martinet</surname>
<given-names>Ludovic</given-names>
</name>
<xref ref-type="aff" rid="A1">1</xref>
<xref ref-type="aff" rid="A9">9</xref>
</contrib>
</contrib-group>
<aff id="A1"><label>1</label>
Immunology of Cancer and Infection Laboratory, QIMR Berghofer Medical Research Institute, Herston, Queensland, Australia.</aff>
<aff id="A2"><label>2</label>
School of Medicine, University of Queensland, Herston, Queensland, Australia.</aff>
<aff id="A3"><label>3</label>
Células Inflamatórias e Neoplásicas group, Universidade Federal do Paraná, Curitiba, Paraná, Brazil.</aff>
<aff id="A4"><label>4</label>
Bone Marrow Transplantation and</aff>
<aff id="A5"><label>5</label>
Cancer Immunoregulation and Immunotherapy Laboratory, QIMR Berghofer Medical Research Institute, Herston, Queensland, Australia.</aff>
<aff id="A6"><label>6</label>
Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, Missouri, USA.</aff>
<aff id="A7"><label>7</label>
Sir Peter MacCallum Department of Oncology, University of Melbourne, Parkville, Victoria, Australia.</aff>
<aff id="A8"><label>8</label>
Comprehensive Cancer Center, Mayo Clinic, Scottsdale, Arizona, USA.</aff>
<aff id="A9"><label>9</label>
INSERM UMR 1037, Cancer Research Center of Toulouse, Toulouse, France.</aff>
<author-notes><corresp>Address correspondence to: Mark J. Smyth, Immunology in Cancer and Infection Laboratory, QIMR Berghofer Medical Research Institute, 300 Herston Road, Herston 4006, Australia. Phone: 61.7.3845.3957; E-mail: <email>mark.smyth@qimrberghofer.edu.au</email>
.</corresp>
<fn><p><bold>Authorship note:</bold>
Camille Guillerey, Lucas Ferrari de Andrade, Mark J. Smyth, and Ludovic Martinet contributed equally to this work.</p>
</fn>
</author-notes>
<pub-date pub-type="epub"><day>20</day>
<month>4</month>
<year>2015</year>
</pub-date>
<pub-date pub-type="ppub"><day>1</day>
<month>5</month>
<year>2015</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>20</day>
<month>4</month>
<year>2015</year>
</pub-date>
<pmc-comment> PMC Release delay is 0 months and 0 days and was based on the
. </pmc-comment>
<volume>125</volume>
<issue>5</issue>
<fpage>2077</fpage>
<lpage>2089</lpage>
<history><date date-type="received"><day>21</day>
<month>5</month>
<year>2014</year>
</date>
<date date-type="accepted"><day>12</day>
<month>3</month>
<year>2015</year>
</date>
</history>
<permissions><copyright-statement>Copyright © 2015, American Society for Clinical Investigation</copyright-statement>
<copyright-year>2015</copyright-year>
<copyright-holder>American Society for Clinical Investigation</copyright-holder>
</permissions>
<abstract><p>Multiple myeloma (MM) is an age-dependent hematological malignancy. Evaluation of immune interactions that drive MM relies on in vitro experiments that do not reflect the complex cellular stroma involved in MM pathogenesis. Here we used Vk*MYC transgenic mice, which spontaneously develop MM, and demonstrated that the immune system plays a critical role in the control of MM progression and the response to treatment. We monitored Vk*MYC mice that had been crossed with <italic>Cd226</italic>
mutant mice over a period of 3 years and found that CD226 limits spontaneous MM development. The CD226-dependent anti-myeloma immune response against transplanted Vk*MYC MM cells was mediated both by NK and CD8<sup>+</sup>
T cells through perforin and IFN-γ pathways. Moreover, CD226 expression was required for optimal antimyeloma efficacy of cyclophosphamide (CTX) and bortezomib (Btz), which are both standardly used to manage MM in patients. Activation of costimulatory receptor CD137 with mAb (4-1BB) exerted strong antimyeloma activity, while inhibition of coinhibitory receptors PD-1 and CTLA-4 had no effect. Taken together, the results of this study provide in vivo evidence that CD226 is important for MM immunosurveillance and indicate that specific immune components should be targeted for optimal MM treatment efficacy. As progressive immunosuppression associates with MM development, strategies aimed to increase immune functions may have important therapeutic implications in MM.</p>
</abstract>
</article-meta>
</front>
</pmc>
</record>
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