RapamycinFungusV1, Main, Curation, bibRecord, 000A75

T cells conditioned with MDSC show an increased anti-tumor activity after adoptive T cell based immunotherapy.

Identifieur interne : 000A75 ( Main/Curation ); précédent : 000A74; suivant : 000A76

T cells conditioned with MDSC show an increased anti-tumor activity after adoptive T cell based immunotherapy.

Auteurs : Patrick L. Raber [États-Unis] ; Rosa A. Sierra [États-Unis] ; Paul T. Thevenot [États-Unis] ; Zhang Shuzhong [États-Unis] ; Dorota D. Wyczechowska [États-Unis] ; Takumi Kumai [États-Unis] ; Esteban Celis [États-Unis] ; Paulo C. Rodriguez [États-Unis]

Source :

Oncotarget [ 1949-2553 ] ; 2016.

RBID : pubmed:27007050

Descripteurs français

English descriptors

KwdEn :
- Animals (MeSH), Carcinoma, Lewis Lung (immunology), Carcinoma, Lewis Lung (therapy), Cell Communication (immunology), Cell Differentiation (immunology), Cell Line, Tumor (MeSH), Female (MeSH), Immunotherapy, Adoptive (methods), Lymphocyte Activation (MeSH), Mice (MeSH), Mice, Inbred C57BL (MeSH), Myeloid Cells (immunology), T-Lymphocytes (immunology), Thymoma (immunology), Thymoma (therapy), Thymus Neoplasms (immunology), Thymus Neoplasms (therapy).
MESH :
- immunology : Carcinoma, Lewis Lung, Cell Communication, Cell Differentiation, Myeloid Cells, T-Lymphocytes, Thymoma, Thymus Neoplasms.
- methods : Immunotherapy, Adoptive.
- therapy : Carcinoma, Lewis Lung, Thymoma, Thymus Neoplasms.
- Animals, Cell Line, Tumor, Female, Lymphocyte Activation, Mice, Mice, Inbred C57BL.

Abstract

The success of adoptive T cell-based immunotherapy (ACT) in cancer is limited in part by the accumulation of myeloid-derived suppressor cells (MDSC), which block several T cell functions, including T cell proliferation and the expression of various cytotoxic mediators. Paradoxically, the inhibition of CD8+ T cell differentiation into cytotoxic populations increased their efficacy after ACT into tumor-bearing hosts. Therefore, we aimed to test the impact of conditioning CD8+ T cells with MDSC on their differentiation potential and ACT efficacy. Our results indicate that MDSC impaired the progression of CD8+ T cells into effector populations, without altering their activation status, production of IL-2, or signaling through the T cell receptor. In addition, culture of CD8+ T cells with MDSC resulted in an increased ACT anti-tumor efficacy, which correlated with a higher frequency of the transferred T cells and elevated IFNγ production. Interestingly, activated CD62L+ CD8+ T cells were responsible for the enhanced anti-tumor activity showed by MDSC-exposed T cells. Additional results showed a decreased protein synthesis rate and lower activity of the mammalian/mechanistic target of rapamycin (mTOR) in T cells conditioned with MDSC. Silencing of the negative mTOR regulator tuberous sclerosis complex-2 in T cells co-cultured with MDSC restored mTOR activity, but resulted in T cell apoptosis. These results indicate that conditioning of T cells with MDSC induces stress survival pathways mediated by a blunted mTOR signaling, which regulated T cell differentiation and ACT efficacy. Continuation of this research will enable the development of better strategies to increase ACT responses in cancer.

DOI: 10.18632/oncotarget.8197
PubMed: 27007050
PubMed Central: PMC4951233

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Le document en format XML

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<author><name sortKey="Wyczechowska, Dorota D" sort="Wyczechowska, Dorota D" uniqKey="Wyczechowska D" first="Dorota D" last="Wyczechowska">Dorota D. Wyczechowska</name>
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<author><name sortKey="Celis, Esteban" sort="Celis, Esteban" uniqKey="Celis E" first="Esteban" last="Celis">Esteban Celis</name>
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</affiliation>
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<author><name sortKey="Rodriguez, Paulo C" sort="Rodriguez, Paulo C" uniqKey="Rodriguez P" first="Paulo C" last="Rodriguez">Paulo C. Rodriguez</name>
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<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Georgia Regents University Cancer Center, Augusta, GA</wicri:regionArea>
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<series><title level="j">Oncotarget</title>
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<imprint><date when="2016" type="published">2016</date>
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<term>Carcinoma, Lewis Lung (immunology)</term>
<term>Carcinoma, Lewis Lung (therapy)</term>
<term>Cell Communication (immunology)</term>
<term>Cell Differentiation (immunology)</term>
<term>Cell Line, Tumor (MeSH)</term>
<term>Female (MeSH)</term>
<term>Immunotherapy, Adoptive (methods)</term>
<term>Lymphocyte Activation (MeSH)</term>
<term>Mice (MeSH)</term>
<term>Mice, Inbred C57BL (MeSH)</term>
<term>Myeloid Cells (immunology)</term>
<term>T-Lymphocytes (immunology)</term>
<term>Thymoma (immunology)</term>
<term>Thymoma (therapy)</term>
<term>Thymus Neoplasms (immunology)</term>
<term>Thymus Neoplasms (therapy)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Activation des lymphocytes (MeSH)</term>
<term>Animaux (MeSH)</term>
<term>Carcinome pulmonaire de Lewis (immunologie)</term>
<term>Carcinome pulmonaire de Lewis (thérapie)</term>
<term>Cellules myéloïdes (immunologie)</term>
<term>Communication cellulaire (immunologie)</term>
<term>Différenciation cellulaire (immunologie)</term>
<term>Femelle (MeSH)</term>
<term>Immunothérapie adoptive (méthodes)</term>
<term>Lignée cellulaire tumorale (MeSH)</term>
<term>Lymphocytes T (immunologie)</term>
<term>Souris (MeSH)</term>
<term>Souris de lignée C57BL (MeSH)</term>
<term>Thymome (immunologie)</term>
<term>Thymome (thérapie)</term>
<term>Tumeurs du thymus (immunologie)</term>
<term>Tumeurs du thymus (thérapie)</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Carcinome pulmonaire de Lewis</term>
<term>Cellules myéloïdes</term>
<term>Communication cellulaire</term>
<term>Différenciation cellulaire</term>
<term>Lymphocytes T</term>
<term>Thymome</term>
<term>Tumeurs du thymus</term>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Carcinoma, Lewis Lung</term>
<term>Cell Communication</term>
<term>Cell Differentiation</term>
<term>Myeloid Cells</term>
<term>T-Lymphocytes</term>
<term>Thymoma</term>
<term>Thymus Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Immunotherapy, Adoptive</term>
</keywords>
<keywords scheme="MESH" qualifier="méthodes" xml:lang="fr"><term>Immunothérapie adoptive</term>
</keywords>
<keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Carcinoma, Lewis Lung</term>
<term>Thymoma</term>
<term>Thymus Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="thérapie" xml:lang="fr"><term>Carcinome pulmonaire de Lewis</term>
<term>Thymome</term>
<term>Tumeurs du thymus</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Cell Line, Tumor</term>
<term>Female</term>
<term>Lymphocyte Activation</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Activation des lymphocytes</term>
<term>Animaux</term>
<term>Femelle</term>
<term>Lignée cellulaire tumorale</term>
<term>Souris</term>
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<front><div type="abstract" xml:lang="en">The success of adoptive T cell-based immunotherapy (ACT) in cancer is limited in part by the accumulation of myeloid-derived suppressor cells (MDSC), which block several T cell functions, including T cell proliferation and the expression of various cytotoxic mediators. Paradoxically, the inhibition of CD8+ T cell differentiation into cytotoxic populations increased their efficacy after ACT into tumor-bearing hosts. Therefore, we aimed to test the impact of conditioning CD8+ T cells with MDSC on their differentiation potential and ACT efficacy. Our results indicate that MDSC impaired the progression of CD8+ T cells into effector populations, without altering their activation status, production of IL-2, or signaling through the T cell receptor. In addition, culture of CD8+ T cells with MDSC resulted in an increased ACT anti-tumor efficacy, which correlated with a higher frequency of the transferred T cells and elevated IFNγ production. Interestingly, activated CD62L+ CD8+ T cells were responsible for the enhanced anti-tumor activity showed by MDSC-exposed T cells. Additional results showed a decreased protein synthesis rate and lower activity of the mammalian/mechanistic target of rapamycin (mTOR) in T cells conditioned with MDSC. Silencing of the negative mTOR regulator tuberous sclerosis complex-2 in T cells co-cultured with MDSC restored mTOR activity, but resulted in T cell apoptosis. These results indicate that conditioning of T cells with MDSC induces stress survival pathways mediated by a blunted mTOR signaling, which regulated T cell differentiation and ACT efficacy. Continuation of this research will enable the development of better strategies to increase ACT responses in cancer.</div>
</front>
</TEI>
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<DateCompleted><Year>2017</Year>
<Month>02</Month>
<Day>10</Day>
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<Month>11</Month>
<Day>13</Day>
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<JournalIssue CitedMedium="Internet"><Volume>7</Volume>
<Issue>14</Issue>
<PubDate><Year>2016</Year>
<Month>Apr</Month>
<Day>05</Day>
</PubDate>
</JournalIssue>
<Title>Oncotarget</Title>
<ISOAbbreviation>Oncotarget</ISOAbbreviation>
</Journal>
<ArticleTitle>T cells conditioned with MDSC show an increased anti-tumor activity after adoptive T cell based immunotherapy.</ArticleTitle>
<Pagination><MedlinePgn>17565-78</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.18632/oncotarget.8197</ELocationID>
<Abstract><AbstractText>The success of adoptive T cell-based immunotherapy (ACT) in cancer is limited in part by the accumulation of myeloid-derived suppressor cells (MDSC), which block several T cell functions, including T cell proliferation and the expression of various cytotoxic mediators. Paradoxically, the inhibition of CD8+ T cell differentiation into cytotoxic populations increased their efficacy after ACT into tumor-bearing hosts. Therefore, we aimed to test the impact of conditioning CD8+ T cells with MDSC on their differentiation potential and ACT efficacy. Our results indicate that MDSC impaired the progression of CD8+ T cells into effector populations, without altering their activation status, production of IL-2, or signaling through the T cell receptor. In addition, culture of CD8+ T cells with MDSC resulted in an increased ACT anti-tumor efficacy, which correlated with a higher frequency of the transferred T cells and elevated IFNγ production. Interestingly, activated CD62L+ CD8+ T cells were responsible for the enhanced anti-tumor activity showed by MDSC-exposed T cells. Additional results showed a decreased protein synthesis rate and lower activity of the mammalian/mechanistic target of rapamycin (mTOR) in T cells conditioned with MDSC. Silencing of the negative mTOR regulator tuberous sclerosis complex-2 in T cells co-cultured with MDSC restored mTOR activity, but resulted in T cell apoptosis. These results indicate that conditioning of T cells with MDSC induces stress survival pathways mediated by a blunted mTOR signaling, which regulated T cell differentiation and ACT efficacy. Continuation of this research will enable the development of better strategies to increase ACT responses in cancer.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Raber</LastName>
<ForeName>Patrick L</ForeName>
<Initials>PL</Initials>
<AffiliationInfo><Affiliation>Adaptive Biotechnologies, Seattle, WA, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Sierra</LastName>
<ForeName>Rosa A</ForeName>
<Initials>RA</Initials>
<AffiliationInfo><Affiliation>Georgia Regents University Cancer Center, Augusta, GA, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Thevenot</LastName>
<ForeName>Paul T</ForeName>
<Initials>PT</Initials>
<AffiliationInfo><Affiliation>Institute of Translational Research, Ochsner Medical Center, New Orleans, LA, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Shuzhong</LastName>
<ForeName>Zhang</ForeName>
<Initials>Z</Initials>
<AffiliationInfo><Affiliation>Georgia Regents University Cancer Center, Augusta, GA, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wyczechowska</LastName>
<ForeName>Dorota D</ForeName>
<Initials>DD</Initials>
<AffiliationInfo><Affiliation>Stanley S. Scott Cancer Center, Louisiana State University Health Sciences Center, New Orleans, LA, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Kumai</LastName>
<ForeName>Takumi</ForeName>
<Initials>T</Initials>
<AffiliationInfo><Affiliation>Georgia Regents University Cancer Center, Augusta, GA, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Celis</LastName>
<ForeName>Esteban</ForeName>
<Initials>E</Initials>
<AffiliationInfo><Affiliation>Georgia Regents University Cancer Center, Augusta, GA, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Rodriguez</LastName>
<ForeName>Paulo C</ForeName>
<Initials>PC</Initials>
<AffiliationInfo><Affiliation>Georgia Regents University Cancer Center, Augusta, GA, USA.</Affiliation>
</AffiliationInfo>
</Author>
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<MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018827" MajorTopicYN="N">Carcinoma, Lewis Lung</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
<QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002450" MajorTopicYN="N">Cell Communication</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002454" MajorTopicYN="N">Cell Differentiation</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D045744" MajorTopicYN="N">Cell Line, Tumor</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D016219" MajorTopicYN="N">Immunotherapy, Adoptive</DescriptorName>
<QualifierName UI="Q000379" MajorTopicYN="Y">methods</QualifierName>
</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="D022423" MajorTopicYN="N">Myeloid Cells</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D013601" MajorTopicYN="N">T-Lymphocytes</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D013945" MajorTopicYN="N">Thymoma</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
<QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D013953" MajorTopicYN="N">Thymus Neoplasms</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
<QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Immune response</Keyword>
<Keyword MajorTopicYN="N">Immunity</Keyword>
<Keyword MajorTopicYN="N">Immunology and Microbiology Section</Keyword>
<Keyword MajorTopicYN="N">adoptive T cell transfer immunotherapy (ACT)</Keyword>
<Keyword MajorTopicYN="N">central memory T cells (TCM)</Keyword>
<Keyword MajorTopicYN="N">mammalian target of rapamycin (mTOR)</Keyword>
<Keyword MajorTopicYN="N">myeloid-derived suppressor cells (MDSC)</Keyword>
<Keyword MajorTopicYN="N">stem cell memory T cells (TSCM)</Keyword>
</KeywordList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2015</Year>
<Month>10</Month>
<Day>20</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2016</Year>
<Month>03</Month>
<Day>14</Day>
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T cells conditioned with MDSC show an increased anti-tumor activity after adoptive T cell based immunotherapy.

T cells conditioned with MDSC show an increased anti-tumor activity after adoptive T cell based immunotherapy.

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