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Université d'Orléans |  |
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Université d'Orléans | |
| HAL : pasteur-00576679, version 1 |
| PubMed : 21383056 |
| PubMed Central : 3058575 |
| DOI : 10.1084/jem.20100269 |
| Fiche détaillée |  Récupérer au format |
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| Journal of Experimental Medicine / The Journal of Experimental Medicine 208, 3 (2011) 491-503 |
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| Contribution of IL-17-producing {gamma}{delta} T cells to the efficacy of anticancer chemotherapy. |
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| Yuting Ma 1, 2Laetitia Aymeric 1, 2 |
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| (14/03/2011) |
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| By triggering immunogenic cell death, some anticancer compounds, including anthracyclines and oxaliplatin, elicit tumor-specific, interferon-γ-producing CD8(+) αβ T lymphocytes (Tc1 CTLs) that are pivotal for an optimal therapeutic outcome. Here, we demonstrate that chemotherapy induces a rapid and prominent invasion of interleukin (IL)-17-producing γδ (Vγ4(+) and Vγ6(+)) T lymphocytes (γδ T17 cells) that precedes the accumulation of Tc1 CTLs within the tumor bed. In T cell receptor δ(-/-) or Vγ4/6(-/-) mice, the therapeutic efficacy of chemotherapy was compromised, no IL-17 was produced by tumor-infiltrating T cells, and Tc1 CTLs failed to invade the tumor after treatment. Although γδ T17 cells could produce both IL-17A and IL-22, the absence of a functional IL-17A-IL-17R pathway significantly reduced tumor-specific T cell responses elicited by tumor cell death, and the efficacy of chemotherapy in four independent transplantable tumor models. Adoptive transfer of γδ T cells restored the efficacy of chemotherapy in IL-17A(-/-) hosts. The anticancer effect of infused γδ T cells was lost when they lacked either IL-1R1 or IL-17A. Conventional helper CD4(+) αβ T cells failed to produce IL-17 after chemotherapy. We conclude that γδ T17 cells play a decisive role in chemotherapy-induced anticancer immune responses. |
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| 1 : | Immunologie des tumeurs et immunothérapie |
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INSERM : U1015 – Institut Gustave Roussy |
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| 2 : | Ecole doctorale de cancérologie |
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Université Paris XI - Paris Sud |
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| 3 : | Cancer immunology program |
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Peter MacCallum Cancer Centre |
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| 4 : | Développement des Lymphocytes |
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INSERM : U668 – Institut Pasteur de Paris |
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| 5 : | Centre Georges-François Leclerc (CGFL) |
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CRLCC Georges-François Leclerc |
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| 6 : | Faculté de Médecine et de Pharmacie |
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Université de Bourgogne |
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| 7 : | Lipides - Nutrition - Cancer |
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INSERM : U866 – Université de Bourgogne |
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| 8 : | Division of Hepatology and Gene Therapy (CIMA) |
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Center for Applied Medical Research |
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| 9 : | Molecular Microbiology Group (COMB) |
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University of the Ruykyus |
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| 10 : | Laboratory of Biological protection |
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Kyoto University |
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| 11 : | Immunologie et Embryologie Moléculaire (IEM) |
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CNRS : FRE2815 – Université d'Orléans |
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| 12 : | Immunologie, génétique et traitement des maladies métaboliques et du diabète |
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INSERM : U561 – Université Paris V - Paris Descartes |
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| 13 : | Apoptose, cancer et immunité |
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INSERM : U848 – Université Paris XI - Paris Sud – Institut Gustave Roussy |
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| 14 : | Département de Biologie et pathologie médicale |
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Institut Gustave Roussy |
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| 15 : | Composantes innées de la réponse immunitaire et différenciation (CIRID) |
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CNRS : UMR5164 – Université Victor Segalen - Bordeaux II |
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| 16 : | CIC - Biotherapie - Igr - Institut Curie |
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INSERM : CBT507 |
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| 17 : | metabolomics platform |
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Institut Gustave Roussy |
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| 18 : | Centre de Recherche des Cordeliers |
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INSERM : U872 – Université Pierre et Marie Curie [UPMC] - Paris VI – Université Paris V - Paris Descartes |
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| 19 : | Pôle de biologie |
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Hôpital européen Georges Pompidou – Assistance publique - Hôpitaux de Paris (AP-HP) |
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| 20 : | Faculté de médecine |
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Université Paris V - Paris Descartes |
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| 21 : | Faculté de médecine |
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Université Paris XI - Paris Sud |
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| domaine | : | Sciences du Vivant/Immunologie |
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| Liste des fichiers attachés à ce document : | ||||||||
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| pasteur-00576679, version 1 | |
| http://hal-pasteur.archives-ouvertes.fr/pasteur-00576679 | |
| oai:hal-pasteur.archives-ouvertes.fr:pasteur-00576679 | |
| Contributeur : Marie-Christine Vougny | |
| Soumis le : Mardi 22 Mars 2011, 12:44:16 | |
| Dernière modification le : Mardi 22 Mars 2011, 12:51:29 | |
