RapamycinFungusV1, Main, Exploration, bibRecord, 000A84

Immune-Stimulatory Effects of Rapamycin Are Mediated by Stimulation of Antitumor γδ T Cells.

Identifieur interne : 000A84 ( Main/Exploration ); précédent : 000A83; suivant : 000A85

Immune-Stimulatory Effects of Rapamycin Are Mediated by Stimulation of Antitumor γδ T Cells.

Auteurs : Vinh Dao [États-Unis] ; Yang Liu [République populaire de Chine] ; Srilakshmi Pandeswara [États-Unis] ; Robert S. Svatek [États-Unis] ; Jonathan A. Gelfond [États-Unis] ; Aijie Liu [États-Unis] ; Vincent Hurez [États-Unis] ; Tyler J. Curiel [États-Unis]

Source :

Cancer research [ 1538-7445 ] ; 2016.

RBID : pubmed:27569211

Descripteurs français

KwdFr :
- 7,12-Diméthyl-benzo[a]anthracène (MeSH), Adjuvants immunologiques (pharmacologie), Animaux (MeSH), Chimiokine CXCL10 (physiologie), Cytotoxicité immunologique (effets des médicaments et des substances chimiques), Femelle (MeSH), Humains (MeSH), Interféron gamma (physiologie), Mouvement cellulaire (MeSH), Récepteur lymphocytaire T antigène, gamma-delta (analyse), Récepteurs CXCR3 (physiologie), Sirolimus (pharmacologie), Souris (MeSH), Souris de lignée C57BL (MeSH), Sous-populations de lymphocytes T (effets des médicaments et des substances chimiques), Sous-populations de lymphocytes T (immunologie), Sérine-thréonine kinases TOR (antagonistes et inhibiteurs), Tumeurs cutanées (prévention et contrôle).
MESH :
- analyse : Récepteur lymphocytaire T antigène, gamma-delta.
- antagonistes et inhibiteurs : Sérine-thréonine kinases TOR.
- effets des médicaments et des substances chimiques : Cytotoxicité immunologique, Sous-populations de lymphocytes T.
- immunologie : Sous-populations de lymphocytes T.
- pharmacologie : Adjuvants immunologiques, Sirolimus.
- physiologie : Chimiokine CXCL10, Interféron gamma, Récepteurs CXCR3.
- prévention et contrôle : Tumeurs cutanées.
- 7,12-Diméthyl-benzo[a]anthracène, Animaux, Femelle, Humains, Mouvement cellulaire, Souris, Souris de lignée C57BL.

English descriptors

KwdEn :
- 9,10-Dimethyl-1,2-benzanthracene (MeSH), Adjuvants, Immunologic (pharmacology), Animals (MeSH), Cell Movement (MeSH), Chemokine CXCL10 (physiology), Cytotoxicity, Immunologic (drug effects), Female (MeSH), Humans (MeSH), Interferon-gamma (physiology), Mice (MeSH), Mice, Inbred C57BL (MeSH), Receptors, Antigen, T-Cell, gamma-delta (analysis), Receptors, CXCR3 (physiology), Sirolimus (pharmacology), Skin Neoplasms (prevention & control), T-Lymphocyte Subsets (drug effects), T-Lymphocyte Subsets (immunology), TOR Serine-Threonine Kinases (antagonists & inhibitors).
MESH :
- chemical , analysis : Receptors, Antigen, T-Cell, gamma-delta.
- chemical , antagonists & inhibitors : TOR Serine-Threonine Kinases.
- chemical , pharmacology : Adjuvants, Immunologic, Sirolimus.
- chemical , physiology : Chemokine CXCL10, Interferon-gamma, Receptors, CXCR3.
- chemical : 9,10-Dimethyl-1,2-benzanthracene.
- drug effects : Cytotoxicity, Immunologic, T-Lymphocyte Subsets.
- immunology : T-Lymphocyte Subsets.
- prevention & control : Skin Neoplasms.
- Animals, Cell Movement, Female, Humans, Mice, Mice, Inbred C57BL.

Abstract

The FDA-approved mTOR inhibitor rapamycin mediates important immune effects, but its contributions to the anticancer effects of the drug are unclear. Here we report evidence that rapamycin-mediated cancer protection relies upon stimulation of γδ T cells. In a well-established mouse model of carcinogen and inflammation-driven skin carcinogenesis, IFNγ recruited γδ TCR^mid T cells to the epidermis where rapamycin boosted their perforin-dependent antitumor properties. These antitumor cells were mostly Vγ5^-Vγ4^-Vγ1^- in phenotype. IFNγ signals were required in both hematopoietic and nonhematopoietic cells for rapamycin to optimally promote epidermal infiltration of γδ TCR^mid T cells, as mediated by CXCR3-CXCL10 interactions, along with the antitumor effects of these cells. In mouse xenograft models of human squamous cell carcinoma, rapamycin improved human γδ T-cell-mediated cancer cell killing. Our results identify immune mechanisms for the cancer prevention and treatment properties of rapamycin, challenging the paradigm that mTOR inhibition acts primarily by direct action on tumor cells. Cancer Res; 76(20); 5970-82. ©2016 AACR.

DOI: 10.1158/0008-5472.CAN-16-0091
PubMed: 27569211
PubMed Central: PMC5065775

Affiliations:

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 000979
to stream Main, to step Curation: 000979

Le document en format XML

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<term>Adjuvants, Immunologic (pharmacology)</term>
<term>Animals (MeSH)</term>
<term>Cell Movement (MeSH)</term>
<term>Chemokine CXCL10 (physiology)</term>
<term>Cytotoxicity, Immunologic (drug effects)</term>
<term>Female (MeSH)</term>
<term>Humans (MeSH)</term>
<term>Interferon-gamma (physiology)</term>
<term>Mice (MeSH)</term>
<term>Mice, Inbred C57BL (MeSH)</term>
<term>Receptors, Antigen, T-Cell, gamma-delta (analysis)</term>
<term>Receptors, CXCR3 (physiology)</term>
<term>Sirolimus (pharmacology)</term>
<term>Skin Neoplasms (prevention & control)</term>
<term>T-Lymphocyte Subsets (drug effects)</term>
<term>T-Lymphocyte Subsets (immunology)</term>
<term>TOR Serine-Threonine Kinases (antagonists & inhibitors)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>7,12-Diméthyl-benzo[a]anthracène (MeSH)</term>
<term>Adjuvants immunologiques (pharmacologie)</term>
<term>Animaux (MeSH)</term>
<term>Chimiokine CXCL10 (physiologie)</term>
<term>Cytotoxicité immunologique (effets des médicaments et des substances chimiques)</term>
<term>Femelle (MeSH)</term>
<term>Humains (MeSH)</term>
<term>Interféron gamma (physiologie)</term>
<term>Mouvement cellulaire (MeSH)</term>
<term>Récepteur lymphocytaire T antigène, gamma-delta (analyse)</term>
<term>Récepteurs CXCR3 (physiologie)</term>
<term>Sirolimus (pharmacologie)</term>
<term>Souris (MeSH)</term>
<term>Souris de lignée C57BL (MeSH)</term>
<term>Sous-populations de lymphocytes T (effets des médicaments et des substances chimiques)</term>
<term>Sous-populations de lymphocytes T (immunologie)</term>
<term>Sérine-thréonine kinases TOR (antagonistes et inhibiteurs)</term>
<term>Tumeurs cutanées (prévention et contrôle)</term>
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<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Adjuvants, Immunologic</term>
<term>Sirolimus</term>
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<keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Chemokine CXCL10</term>
<term>Interferon-gamma</term>
<term>Receptors, CXCR3</term>
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</keywords>
<keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Sérine-thréonine kinases TOR</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cytotoxicity, Immunologic</term>
<term>T-Lymphocyte Subsets</term>
</keywords>
<keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Cytotoxicité immunologique</term>
<term>Sous-populations de lymphocytes T</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Sous-populations de lymphocytes T</term>
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<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>T-Lymphocyte Subsets</term>
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<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Adjuvants immunologiques</term>
<term>Sirolimus</term>
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<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Chimiokine CXCL10</term>
<term>Interféron gamma</term>
<term>Récepteurs CXCR3</term>
</keywords>
<keywords scheme="MESH" qualifier="prevention & control" xml:lang="en"><term>Skin Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="prévention et contrôle" xml:lang="fr"><term>Tumeurs cutanées</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Cell Movement</term>
<term>Female</term>
<term>Humans</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
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<keywords scheme="MESH" xml:lang="fr"><term>7,12-Diméthyl-benzo[a]anthracène</term>
<term>Animaux</term>
<term>Femelle</term>
<term>Humains</term>
<term>Mouvement cellulaire</term>
<term>Souris</term>
<term>Souris de lignée C57BL</term>
</keywords>
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<front><div type="abstract" xml:lang="en">The FDA-approved mTOR inhibitor rapamycin mediates important immune effects, but its contributions to the anticancer effects of the drug are unclear. Here we report evidence that rapamycin-mediated cancer protection relies upon stimulation of γδ T cells. In a well-established mouse model of carcinogen and inflammation-driven skin carcinogenesis, IFNγ recruited γδ TCR<sup>mid</sup>
 T cells to the epidermis where rapamycin boosted their perforin-dependent antitumor properties. These antitumor cells were mostly Vγ5<sup>-</sup>
Vγ4<sup>-</sup>
Vγ1<sup>-</sup>
 in phenotype. IFNγ signals were required in both hematopoietic and nonhematopoietic cells for rapamycin to optimally promote epidermal infiltration of γδ TCR<sup>mid</sup>
 T cells, as mediated by CXCR3-CXCL10 interactions, along with the antitumor effects of these cells. In mouse xenograft models of human squamous cell carcinoma, rapamycin improved human γδ T-cell-mediated cancer cell killing. Our results identify immune mechanisms for the cancer prevention and treatment properties of rapamycin, challenging the paradigm that mTOR inhibition acts primarily by direct action on tumor cells. Cancer Res; 76(20); 5970-82. ©2016 AACR.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27569211</PMID>
<DateCompleted><Year>2017</Year>
<Month>08</Month>
<Day>07</Day>
</DateCompleted>
<DateRevised><Year>2018</Year>
<Month>11</Month>
<Day>13</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1538-7445</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>76</Volume>
<Issue>20</Issue>
<PubDate><Year>2016</Year>
<Month>10</Month>
<Day>15</Day>
</PubDate>
</JournalIssue>
<Title>Cancer research</Title>
<ISOAbbreviation>Cancer Res</ISOAbbreviation>
</Journal>
<ArticleTitle>Immune-Stimulatory Effects of Rapamycin Are Mediated by Stimulation of Antitumor γδ T Cells.</ArticleTitle>
<Pagination><MedlinePgn>5970-5982</MedlinePgn>
</Pagination>
<Abstract><AbstractText>The FDA-approved mTOR inhibitor rapamycin mediates important immune effects, but its contributions to the anticancer effects of the drug are unclear. Here we report evidence that rapamycin-mediated cancer protection relies upon stimulation of γδ T cells. In a well-established mouse model of carcinogen and inflammation-driven skin carcinogenesis, IFNγ recruited γδ TCR<sup>mid</sup>
 T cells to the epidermis where rapamycin boosted their perforin-dependent antitumor properties. These antitumor cells were mostly Vγ5<sup>-</sup>
Vγ4<sup>-</sup>
Vγ1<sup>-</sup>
 in phenotype. IFNγ signals were required in both hematopoietic and nonhematopoietic cells for rapamycin to optimally promote epidermal infiltration of γδ TCR<sup>mid</sup>
 T cells, as mediated by CXCR3-CXCL10 interactions, along with the antitumor effects of these cells. In mouse xenograft models of human squamous cell carcinoma, rapamycin improved human γδ T-cell-mediated cancer cell killing. Our results identify immune mechanisms for the cancer prevention and treatment properties of rapamycin, challenging the paradigm that mTOR inhibition acts primarily by direct action on tumor cells. Cancer Res; 76(20); 5970-82. ©2016 AACR.</AbstractText>
<CopyrightInformation>©2016 American Association for Cancer Research.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Dao</LastName>
<ForeName>Vinh</ForeName>
<Initials>V</Initials>
<AffiliationInfo><Affiliation>Department of Microbiology and Immunology, University of Texas Health Science Center, San Antonio (UTHSCSA), San Antonio, Texas. Department of Medicine, UTHSCSA, San Antonio, Texas.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Liu</LastName>
<ForeName>Yang</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Department of Medicine, UTHSCSA, San Antonio, Texas. Xiangya School of Medicine, Central South University, Changsha, Hunan, P.R. China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Pandeswara</LastName>
<ForeName>Srilakshmi</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Department of Medicine, UTHSCSA, San Antonio, Texas.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Svatek</LastName>
<ForeName>Robert S</ForeName>
<Initials>RS</Initials>
<AffiliationInfo><Affiliation>Cancer Therapy & Research Center, UTHSCSA, San Antonio, Texas. Department of Urology, UTHSCSA, San Antonio, Texas.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Gelfond</LastName>
<ForeName>Jonathan A</ForeName>
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Immune-Stimulatory Effects of Rapamycin Are Mediated by Stimulation of Antitumor γδ T Cells.

Immune-Stimulatory Effects of Rapamycin Are Mediated by Stimulation of Antitumor γδ T Cells.

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