CCL2/CCR2-dependent recruitment of functional antigen-presenting cells into tumors upon chemotherapy.
Identifieur interne : 003917 ( PubMed/Curation ); précédent : 003916; suivant : 003918CCL2/CCR2-dependent recruitment of functional antigen-presenting cells into tumors upon chemotherapy.
Auteurs : Yuting Ma [Allemagne] ; Stephen R. Mattarollo ; Sandy Adjemian ; Heng Yang ; Laetitia Aymeric ; Dalil Hannani ; João Paulo Portela Catani ; Helene Duret ; Michele W L. Teng ; Oliver Kepp ; Yidan Wang ; Antonella Sistigu ; Joachim L. Schultze ; Gautier Stoll ; Lorenzo Galluzzi ; Laurence Zitvogel ; Mark J. Smyth ; Guido KroemerSource :
- Cancer research [ 1538-7445 ] ; 2014.
Descripteurs français
- KwdFr :
- Activation des lymphocytes, Animaux, Anthracyclines (usage thérapeutique), Antigènes néoplasiques (métabolisme), Antinéoplasiques (usage thérapeutique), Cellules dendritiques (cytologie), Cellules présentatrices d'antigène (), Cellules présentatrices d'antigène (immunologie), Chimiokine CCL2 (génétique), Chimiokine CCL2 (métabolisme), Cytométrie en flux, Femelle, Lignée cellulaire tumorale, Lymphadénectomie, Lymphocytes T (cytologie), Microscopie de fluorescence, Présentation d'antigène, Récepteurs CCR2 (métabolisme), Souris, Souris de lignée C57BL, Souris transgéniques, Séquençage par oligonucléotides en batterie, Transduction du signal, Transplantation tumorale, Tumeurs (traitement médicamenteux).
- MESH :
- cytologie : Cellules dendritiques, Lymphocytes T.
- génétique : Chimiokine CCL2.
- immunologie : Cellules présentatrices d'antigène.
- métabolisme : Antigènes néoplasiques, Chimiokine CCL2, Récepteurs CCR2.
- traitement médicamenteux : Tumeurs.
- usage thérapeutique : Anthracyclines, Antinéoplasiques.
- Activation des lymphocytes, Animaux, Cellules présentatrices d'antigène, Cytométrie en flux, Femelle, Lignée cellulaire tumorale, Lymphadénectomie, Microscopie de fluorescence, Présentation d'antigène, Souris, Souris de lignée C57BL, Souris transgéniques, Séquençage par oligonucléotides en batterie, Transduction du signal, Transplantation tumorale.
English descriptors
- KwdEn :
- Animals, Anthracyclines (therapeutic use), Antigen Presentation, Antigen-Presenting Cells (drug effects), Antigen-Presenting Cells (immunology), Antigens, Neoplasm (metabolism), Antineoplastic Agents (therapeutic use), Cell Line, Tumor, Chemokine CCL2 (genetics), Chemokine CCL2 (metabolism), Dendritic Cells (cytology), Female, Flow Cytometry, Lymph Node Excision, Lymphocyte Activation, Mice, Mice, Inbred C57BL, Mice, Transgenic, Microscopy, Fluorescence, Neoplasm Transplantation, Neoplasms (drug therapy), Oligonucleotide Array Sequence Analysis, Receptors, CCR2 (metabolism), Signal Transduction, T-Lymphocytes (cytology).
- MESH :
- chemical , genetics : Chemokine CCL2.
- chemical , metabolism : Antigens, Neoplasm, Chemokine CCL2, Receptors, CCR2.
- chemical , therapeutic use : Anthracyclines, Antineoplastic Agents.
- cytology : Dendritic Cells, T-Lymphocytes.
- drug effects : Antigen-Presenting Cells.
- drug therapy : Neoplasms.
- immunology : Antigen-Presenting Cells.
- Animals, Antigen Presentation, Cell Line, Tumor, Female, Flow Cytometry, Lymph Node Excision, Lymphocyte Activation, Mice, Mice, Inbred C57BL, Mice, Transgenic, Microscopy, Fluorescence, Neoplasm Transplantation, Oligonucleotide Array Sequence Analysis, Signal Transduction.
Abstract
The therapeutic efficacy of anthracyclines relies, at least partially, on the induction of a dendritic cell- and T-lymphocyte-dependent anticancer immune response. Here, we show that anthracycline-based chemotherapy promotes the recruitment of functional CD11b(+)CD11c(+)Ly6C(high)Ly6G(-)MHCII(+) dendritic cell-like antigen-presenting cells (APC) into the tumor bed, but not into lymphoid organs. Accordingly, draining lymph nodes turned out to be dispensable for the proliferation of tumor antigen-specific T cells within neoplastic lesions as induced by anthracyclines. In addition, we found that tumors treated with anthracyclines manifest increased expression levels of the chemokine Ccl2. Such a response is important as neoplasms growing in Ccl2(-/-) mice failed to accumulate dendritic cell-like APCs in response to chemotherapy. Moreover, cancers developing in mice lacking Ccl2 or its receptor (Ccr2) exhibited suboptimal therapeutic responses to anthracycline-based chemotherapy. Altogether, our results underscore the importance of the CCL2/CCR2 signaling axis for therapeutic anticancer immune responses as elicited by immunogenic chemotherapy.
DOI: 10.1158/0008-5472.CAN-13-1265
PubMed: 24302580
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<author><name sortKey="Wang, Yidan" sort="Wang, Yidan" uniqKey="Wang Y" first="Yidan" last="Wang">Yidan Wang</name>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term>
<term>Anthracyclines (therapeutic use)</term>
<term>Antigen Presentation</term>
<term>Antigen-Presenting Cells (drug effects)</term>
<term>Antigen-Presenting Cells (immunology)</term>
<term>Antigens, Neoplasm (metabolism)</term>
<term>Antineoplastic Agents (therapeutic use)</term>
<term>Cell Line, Tumor</term>
<term>Chemokine CCL2 (genetics)</term>
<term>Chemokine CCL2 (metabolism)</term>
<term>Dendritic Cells (cytology)</term>
<term>Female</term>
<term>Flow Cytometry</term>
<term>Lymph Node Excision</term>
<term>Lymphocyte Activation</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>Mice, Transgenic</term>
<term>Microscopy, Fluorescence</term>
<term>Neoplasm Transplantation</term>
<term>Neoplasms (drug therapy)</term>
<term>Oligonucleotide Array Sequence Analysis</term>
<term>Receptors, CCR2 (metabolism)</term>
<term>Signal Transduction</term>
<term>T-Lymphocytes (cytology)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Activation des lymphocytes</term>
<term>Animaux</term>
<term>Anthracyclines (usage thérapeutique)</term>
<term>Antigènes néoplasiques (métabolisme)</term>
<term>Antinéoplasiques (usage thérapeutique)</term>
<term>Cellules dendritiques (cytologie)</term>
<term>Cellules présentatrices d'antigène ()</term>
<term>Cellules présentatrices d'antigène (immunologie)</term>
<term>Chimiokine CCL2 (génétique)</term>
<term>Chimiokine CCL2 (métabolisme)</term>
<term>Cytométrie en flux</term>
<term>Femelle</term>
<term>Lignée cellulaire tumorale</term>
<term>Lymphadénectomie</term>
<term>Lymphocytes T (cytologie)</term>
<term>Microscopie de fluorescence</term>
<term>Présentation d'antigène</term>
<term>Récepteurs CCR2 (métabolisme)</term>
<term>Souris</term>
<term>Souris de lignée C57BL</term>
<term>Souris transgéniques</term>
<term>Séquençage par oligonucléotides en batterie</term>
<term>Transduction du signal</term>
<term>Transplantation tumorale</term>
<term>Tumeurs (traitement médicamenteux)</term>
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<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Chemokine CCL2</term>
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<term>Chemokine CCL2</term>
<term>Receptors, CCR2</term>
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<term>Antineoplastic Agents</term>
</keywords>
<keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Cellules dendritiques</term>
<term>Lymphocytes T</term>
</keywords>
<keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Dendritic Cells</term>
<term>T-Lymphocytes</term>
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<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Antigen-Presenting Cells</term>
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<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Neoplasms</term>
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<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Antigen-Presenting Cells</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Antigènes néoplasiques</term>
<term>Chimiokine CCL2</term>
<term>Récepteurs CCR2</term>
</keywords>
<keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Tumeurs</term>
</keywords>
<keywords scheme="MESH" qualifier="usage thérapeutique" xml:lang="fr"><term>Anthracyclines</term>
<term>Antinéoplasiques</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Antigen Presentation</term>
<term>Cell Line, Tumor</term>
<term>Female</term>
<term>Flow Cytometry</term>
<term>Lymph Node Excision</term>
<term>Lymphocyte Activation</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>Mice, Transgenic</term>
<term>Microscopy, Fluorescence</term>
<term>Neoplasm Transplantation</term>
<term>Oligonucleotide Array Sequence Analysis</term>
<term>Signal Transduction</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Activation des lymphocytes</term>
<term>Animaux</term>
<term>Cellules présentatrices d'antigène</term>
<term>Cytométrie en flux</term>
<term>Femelle</term>
<term>Lignée cellulaire tumorale</term>
<term>Lymphadénectomie</term>
<term>Microscopie de fluorescence</term>
<term>Présentation d'antigène</term>
<term>Souris</term>
<term>Souris de lignée C57BL</term>
<term>Souris transgéniques</term>
<term>Séquençage par oligonucléotides en batterie</term>
<term>Transduction du signal</term>
<term>Transplantation tumorale</term>
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<front><div type="abstract" xml:lang="en">The therapeutic efficacy of anthracyclines relies, at least partially, on the induction of a dendritic cell- and T-lymphocyte-dependent anticancer immune response. Here, we show that anthracycline-based chemotherapy promotes the recruitment of functional CD11b(+)CD11c(+)Ly6C(high)Ly6G(-)MHCII(+) dendritic cell-like antigen-presenting cells (APC) into the tumor bed, but not into lymphoid organs. Accordingly, draining lymph nodes turned out to be dispensable for the proliferation of tumor antigen-specific T cells within neoplastic lesions as induced by anthracyclines. In addition, we found that tumors treated with anthracyclines manifest increased expression levels of the chemokine Ccl2. Such a response is important as neoplasms growing in Ccl2(-/-) mice failed to accumulate dendritic cell-like APCs in response to chemotherapy. Moreover, cancers developing in mice lacking Ccl2 or its receptor (Ccr2) exhibited suboptimal therapeutic responses to anthracycline-based chemotherapy. Altogether, our results underscore the importance of the CCL2/CCR2 signaling axis for therapeutic anticancer immune responses as elicited by immunogenic chemotherapy.</div>
</front>
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<Abstract><AbstractText>The therapeutic efficacy of anthracyclines relies, at least partially, on the induction of a dendritic cell- and T-lymphocyte-dependent anticancer immune response. Here, we show that anthracycline-based chemotherapy promotes the recruitment of functional CD11b(+)CD11c(+)Ly6C(high)Ly6G(-)MHCII(+) dendritic cell-like antigen-presenting cells (APC) into the tumor bed, but not into lymphoid organs. Accordingly, draining lymph nodes turned out to be dispensable for the proliferation of tumor antigen-specific T cells within neoplastic lesions as induced by anthracyclines. In addition, we found that tumors treated with anthracyclines manifest increased expression levels of the chemokine Ccl2. Such a response is important as neoplasms growing in Ccl2(-/-) mice failed to accumulate dendritic cell-like APCs in response to chemotherapy. Moreover, cancers developing in mice lacking Ccl2 or its receptor (Ccr2) exhibited suboptimal therapeutic responses to anthracycline-based chemotherapy. Altogether, our results underscore the importance of the CCL2/CCR2 signaling axis for therapeutic anticancer immune responses as elicited by immunogenic chemotherapy.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ma</LastName>
<ForeName>Yuting</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Authors' Affiliations: INSERM, U848; Institut Gustave Roussy; INSERM, U1015, CBT1017; Metabolomics and Cell Biology Platforms, Institut Gustave Roussy, Villejuif, France; Université Paris Descartes/Paris V, Sorbonne Paris Cité; Equipe 11 labellisée par la Ligue Nationale contre le Cancer, Centre de Recherche des Cordeliers, Paris; Université Paris Sud/Paris XI; Le Kremlin Bicêtre; Pôle de Biologie, Hôpital Européen Georges Pompidou, AP-HP; Paris; INSERM, UMR 996, LabEx LERMIT, Clamart, France; Cancer Immunology Program, Peter MacCallum Cancer Centre, East Melbourne, Victoria; Diamantina Institute; School of Medicine, University of Queensland; Immunology in Cancer and Infection Laboratory, QIMR Berghofer Medical Research Institute; Cancer Immunoregulation and Immunotherapy Laboratory, QIMR Berghofer Medical Research Institute, Herston, Queensland, Australia; Laboratorio de Vetores Virais, Instituto do Coração, FM-USP, São Paulo, Brazil; and Genomics & Immunoregulation, LIMES-Institute, University of Bonn, Bonn, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Mattarollo</LastName>
<ForeName>Stephen R</ForeName>
<Initials>SR</Initials>
</Author>
<Author ValidYN="Y"><LastName>Adjemian</LastName>
<ForeName>Sandy</ForeName>
<Initials>S</Initials>
</Author>
<Author ValidYN="Y"><LastName>Yang</LastName>
<ForeName>Heng</ForeName>
<Initials>H</Initials>
</Author>
<Author ValidYN="Y"><LastName>Aymeric</LastName>
<ForeName>Laetitia</ForeName>
<Initials>L</Initials>
</Author>
<Author ValidYN="Y"><LastName>Hannani</LastName>
<ForeName>Dalil</ForeName>
<Initials>D</Initials>
</Author>
<Author ValidYN="Y"><LastName>Portela Catani</LastName>
<ForeName>João Paulo</ForeName>
<Initials>JP</Initials>
</Author>
<Author ValidYN="Y"><LastName>Duret</LastName>
<ForeName>Helene</ForeName>
<Initials>H</Initials>
</Author>
<Author ValidYN="Y"><LastName>Teng</LastName>
<ForeName>Michele W L</ForeName>
<Initials>MW</Initials>
</Author>
<Author ValidYN="Y"><LastName>Kepp</LastName>
<ForeName>Oliver</ForeName>
<Initials>O</Initials>
</Author>
<Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Yidan</ForeName>
<Initials>Y</Initials>
</Author>
<Author ValidYN="Y"><LastName>Sistigu</LastName>
<ForeName>Antonella</ForeName>
<Initials>A</Initials>
</Author>
<Author ValidYN="Y"><LastName>Schultze</LastName>
<ForeName>Joachim L</ForeName>
<Initials>JL</Initials>
</Author>
<Author ValidYN="Y"><LastName>Stoll</LastName>
<ForeName>Gautier</ForeName>
<Initials>G</Initials>
</Author>
<Author ValidYN="Y"><LastName>Galluzzi</LastName>
<ForeName>Lorenzo</ForeName>
<Initials>L</Initials>
</Author>
<Author ValidYN="Y"><LastName>Zitvogel</LastName>
<ForeName>Laurence</ForeName>
<Initials>L</Initials>
</Author>
<Author ValidYN="Y"><LastName>Smyth</LastName>
<ForeName>Mark J</ForeName>
<Initials>MJ</Initials>
</Author>
<Author ValidYN="Y"><LastName>Kroemer</LastName>
<ForeName>Guido</ForeName>
<Initials>G</Initials>
</Author>
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<Language>eng</Language>
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<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
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<ArticleDate DateType="Electronic"><Year>2013</Year>
<Month>12</Month>
<Day>03</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>Cancer Res</MedlineTA>
<NlmUniqueID>2984705R</NlmUniqueID>
<ISSNLinking>0008-5472</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D018943">Anthracyclines</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000951">Antigens, Neoplasm</NameOfSubstance>
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<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000970">Antineoplastic Agents</NameOfSubstance>
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<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C491768">Ccl2 protein, mouse</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C515335">Ccr2 protein, mouse</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D018932">Chemokine CCL2</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D054390">Receptors, CCR2</NameOfSubstance>
</Chemical>
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<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
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<QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D017951" MajorTopicYN="N">Antigen Presentation</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000938" MajorTopicYN="N">Antigen-Presenting Cells</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
<QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000951" MajorTopicYN="N">Antigens, Neoplasm</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
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<QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D045744" MajorTopicYN="N">Cell Line, Tumor</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018932" MajorTopicYN="N">Chemokine CCL2</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D003713" MajorTopicYN="N">Dendritic Cells</DescriptorName>
<QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005434" MajorTopicYN="N">Flow Cytometry</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008197" MajorTopicYN="N">Lymph Node Excision</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008213" MajorTopicYN="N">Lymphocyte Activation</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008822" MajorTopicYN="N">Mice, Transgenic</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008856" MajorTopicYN="N">Microscopy, Fluorescence</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D009368" MajorTopicYN="N">Neoplasm Transplantation</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D009369" MajorTopicYN="N">Neoplasms</DescriptorName>
<QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D020411" MajorTopicYN="N">Oligonucleotide Array Sequence Analysis</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D054390" MajorTopicYN="N">Receptors, CCR2</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D013601" MajorTopicYN="N">T-Lymphocytes</DescriptorName>
<QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName>
</MeshHeading>
</MeshHeadingList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2013</Year>
<Month>12</Month>
<Day>5</Day>
<Hour>6</Hour>
<Minute>0</Minute>
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<PubMedPubDate PubStatus="pubmed"><Year>2013</Year>
<Month>12</Month>
<Day>5</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline"><Year>2014</Year>
<Month>3</Month>
<Day>19</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
</History>
<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList><ArticleId IdType="pubmed">24302580</ArticleId>
<ArticleId IdType="pii">0008-5472.CAN-13-1265</ArticleId>
<ArticleId IdType="doi">10.1158/0008-5472.CAN-13-1265</ArticleId>
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