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5 results on '"Yuting Ma"'

1. CCL2/CCR2-Dependent Recruitment of Functional Antigen-Presenting Cells into Tumors upon Chemotherapy

Author

Antonella Sistigu, Sandy Adjemian, João Paulo Portela Catani, Gautier Stoll, Laetitia Aymeric, Heng Yang, Lorenzo Galluzzi, Dalil Hannani, Yuting Ma, Joachim L. Schultze, Helene Duret, Stephen R. Mattarollo, Guido Kroemer, Laurence Zitvogel, Oliver Kepp, Michele W.L. Teng, Mark J. Smyth, Yidan Wang, Immunologie des tumeurs et immunothérapie (UMR 1015), Université Paris-Sud - Paris 11 (UP11)-Institut Gustave Roussy (IGR)-Institut National de la Santé et de la Recherche Médicale (INSERM), Apoptose, cancer et immunité (U848), Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Gustave Roussy (IGR)-Université Paris-Sud - Paris 11 (UP11), Université Paris 1 Panthéon-Sorbonne - UFR Histoire (UP1 UFR09), Université Paris 1 Panthéon-Sorbonne (UP1), Apoptose, cancer et immunité (Equipe labellisée Ligue contre le cancer - CRC - Inserm U1138), Institut Gustave Roussy (IGR)-Centre de Recherche des Cordeliers (CRC (UMR_S_1138 / U1138)), École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), Plateforme de métabolomique, Direction de la recherche [Gustave Roussy], Institut Gustave Roussy (IGR)-Institut Gustave Roussy (IGR), Centre de Recherche des Cordeliers (CRC), Université Paris Diderot - Paris 7 (UPD7)-École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), National Cancer Institute Regina Elena [Rome, Italy], Life and Medical Sciences Institute for Genomics and Immunoregulation, University of Bonn, Cancer et génome: Bioinformatique, biostatistiques et épidémiologie d'un système complexe, MINES ParisTech - École nationale supérieure des mines de Paris, Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut Curie [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut Gustave Roussy (IGR), Université Paris-Sud - Paris 11 (UP11), Université Paris 1 Panthéon-Sorbonne - École d'Histoire (UP1 UFR09), École Pratique des Hautes Études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-École Pratique des Hautes Études (EPHE), Université Pierre et Marie Curie - Paris 6 (UPMC)-École Pratique des Hautes Études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Universität Bonn = University of Bonn, Mines Paris - PSL (École nationale supérieure des mines de Paris), Université Panthéon-Sorbonne - UFR Histoire (UP1 UFR09), Université Panthéon-Sorbonne (UP1), École pratique des hautes études (EPHE)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-École pratique des hautes études (EPHE)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), Université Paris Diderot - Paris 7 (UPD7)-École pratique des hautes études (EPHE)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Cancer et génôme: Bioinformatique, biostatistiques et épidémiologie d'un système complexe, and MINES ParisTech - École nationale supérieure des mines de Paris-Institut Curie-Institut National de la Santé et de la Recherche Médicale (INSERM)

Subjects
Cancer Research, Chemokine, Anthracycline, Receptors, CCR2, T-Lymphocytes, Antigen presentation, Antigen-Presenting Cells, Antineoplastic Agents, Mice, Transgenic, [SDV.CAN]Life Sciences [q-bio]/Cancer, Lymphocyte Activation, Mice, Immune system, Antigen, Antigens, Neoplasm, Cell Line, Tumor, Neoplasms, Animals, Medicine, Anthracyclines, Antigen-presenting cell, Chemokine CCL2, ComputingMilieux_MISCELLANEOUS, Oligonucleotide Array Sequence Analysis, Antigen Presentation, biology, business.industry, Dendritic Cells, [SDV.IMM.IMM]Life Sciences [q-bio]/Immunology/Immunotherapy, Dendritic cell, Flow Cytometry, 3. Good health, Mice, Inbred C57BL, Lymphatic system, Microscopy, Fluorescence, Oncology, Immunology, Cancer research, biology.protein, Lymph Node Excision, [SDV.IMM]Life Sciences [q-bio]/Immunology, Female, business, Neoplasm Transplantation, 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+Ly6ChighLy6G−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. Cancer Res; 74(2); 436–45. ©2013 AACR.

Published
2014

2. Anticancer Chemotherapy-Induced Intratumoral Recruitment and Differentiation of Antigen-Presenting Cells

Author

Dalil Hannani, Yuting Ma, Erika Vacchelli, Mickaël Michaud, Frédéric Schlemmer, Eric Solary, Laetitia Aymeric, Guido Kroemer, Oliver Kepp, Lorenzo Galluzzi, Laurie Menger, Laurence Zitvogel, Nathalie Droin, Helene Duret, Sandy Adjemian, Takahiro Yamazaki, Heng Yang, Isabelle Martins, Siamon Gordon, Kim Steegh, Mark J. Smyth, Roman Krzysiek, João Paulo Portela Catani, Abdul Qader Sukkurwala, Stephen R. Mattarollo, Philip R. Taylor, Peter van Endert, Immunologie des tumeurs et immunothérapie (UMR 1015), Université Paris-Sud - Paris 11 (UP11)-Institut Gustave Roussy (IGR)-Institut National de la Santé et de la Recherche Médicale (INSERM), Apoptose, cancer et immunité (U848), Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Gustave Roussy (IGR)-Université Paris-Sud - Paris 11 (UP11), Université Paris 1 Panthéon-Sorbonne - UFR Histoire (UP1 UFR09), Université Paris 1 Panthéon-Sorbonne (UP1), Bio-Indicateurs Actuels et Fossiles (BIAF), Université d'Angers (UA), Apoptose, cancer et immunité (Equipe labellisée Ligue contre le cancer - CRC - Inserm U1138), Institut Gustave Roussy (IGR)-Centre de Recherche des Cordeliers (CRC (UMR_S_1138 / U1138)), École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), Institut Gustave Roussy (IGR)-Centre de Recherche des Cordeliers (CRC), Université Paris Diderot - Paris 7 (UPD7)-École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Diderot - Paris 7 (UPD7)-École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre de Recherches Juridiques de l'Université de Franche-Comté - UFC (EA 3225) (CRJFC), Université de Franche-Comté (UFC), Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université Bourgogne Franche-Comté [COMUE] (UBFC), Institut Gustave Roussy (IGR), Service de microbiologie, immunologie biologique, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-AP-HP - Hôpital Antoine Béclère [Clamart], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Sir William Dunn School of Pathology [Oxford], University of Oxford [Oxford], Hématopoïèse normale et pathologique, Université Paris-Sud - Paris 11 (UP11), Plateforme de métabolomique, Direction de la recherche [Gustave Roussy], Institut Gustave Roussy (IGR)-Institut Gustave Roussy (IGR), Université Panthéon-Sorbonne - UFR Histoire (UP1 UFR09), Université Panthéon-Sorbonne (UP1), Département de Géologie, Laboratoire d'étude des bio-indicateurs actuels et fossiles EA2644, École pratique des hautes études (EPHE)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-École pratique des hautes études (EPHE)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), Université Paris Diderot - Paris 7 (UPD7)-École pratique des hautes études (EPHE)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Diderot - Paris 7 (UPD7)-École pratique des hautes études (EPHE)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université de Franche-Comté (UFC), Université Paris-Sud - Paris 11 (UP11)-Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Hôpital Antoine Béclère, Université Paris 1 Panthéon-Sorbonne - École d'Histoire (UP1 UFR09), École Pratique des Hautes Études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-École Pratique des Hautes Études (EPHE), Université Pierre et Marie Curie - Paris 6 (UPMC)-École Pratique des Hautes Études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-École Pratique des Hautes Études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre de Recherches Juridiques de l'Université de Franche-Comté - UFC (UR 3225) (CRJFC), and University of Oxford

Subjects
Adoptive cell transfer, Antigen presentation, Immunology, Antigen-Presenting Cells, Antineoplastic Agents, Apoptosis, [SDV.CAN]Life Sciences [q-bio]/Cancer, Monocyte-Macrophage Precursor Cells, Mice, 03 medical and health sciences, Interleukin 21, 0302 clinical medicine, Antigen, Antigens, Neoplasm, Cell Movement, Nucleotidases, Cell Line, Tumor, Animals, Antigens, Ly, Medicine, Immunology and Allergy, Anthracyclines, Granulocyte Precursor Cells, IL-2 receptor, Antigen-presenting cell, 030304 developmental biology, Immunity, Cellular, 0303 health sciences, CD11b Antigen, CD40, biology, business.industry, Receptors, Purinergic, Cell Differentiation, Dendritic Cells, Neoplasms, Experimental, [SDV.IMM.IMM]Life Sciences [q-bio]/Immunology/Immunotherapy, Adoptive Transfer, CD11c Antigen, 3. Good health, Mice, Inbred C57BL, Infectious Diseases, 030220 oncology & carcinogenesis, biology.protein, Interleukin 12, [SDV.IMM]Life Sciences [q-bio]/Immunology, business
Abstract

International audience; The therapeutic efficacy of anthracyclines relies on antitumor immune responses elicited by dying cancer cells. How chemotherapy-induced cell death leads to efficient antigen presentation to T cells, however, remains a conundrum. We found that intra-tumoral CD11c + CD11b + Ly6C hi cells, which displayed some characteristics of inflammatory dendritic cells and included granulomonocytic precursors, were crucial for anthracycline-induced anticancer immune responses. ATP released by dying cancer cells recruited myeloid cells into tumors and stimulated the local differentiation of CD11c + CD11b + Ly6C hi cells. Such cells efficiently engulfed tumor antigens in situ and presented them to T lymphocytes, thus vaccinating mice, upon adoptive transfer, against a challenge with cancer cells. Manipulations preventing tumor infiltration by CD11c + CD11b + Ly6C hi cells, such as the local overexpression of ectonu-cleotidases, the blockade of purinergic receptors, or the neutralization of CD11b, abolished the immune system-dependent antitumor activity of anthracyclines. Our results identify a subset of tumor-infiltrating leukocytes as therapy-relevant antigen-presenting cells.

Published
2013
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3. Chemotherapy-induced antitumor immunity requires formyl peptide receptor 1

Author

Guido Kroemer, Oliver Kepp, Fabrice Andre, Patrick Günther, José Manuel Bravo-San Pedro, Thomas Ulas, Sandy Adjemian, Elisa E. Baracco, Adele De Ninno, Gwenola Manic, Luca Businaro, Ilio Vitale, Valeria Lucarini, Monica Lucattelli, Federico Pietrocola, Suzette Delaloge, Laurence Zitvogel, Yuting Ma, Joachim L. Schultze, Michaela Semeraro, Giovanna Schiavoni, Celine Lefebvre, Heng Yang, Kariman Chaba, Lionel Apetoh, Antonella Sistigu, Sylvain Ladoire, Gautier Stoll, Christophe Borg, David Enot, Valérie Boige, Michel Ducreux, Francesca Castoldi, Francesca Peschiaroli, Fabrizio Mattei, Sylvie Rusakiewicz, Erika Vacchelli, Cécile Delarasse, Michele Signore, Annamaria Gerardino, Claire Mulot, and Pierre Laurent-Puig

Subjects
Anthracycline, Colorectal cancer, medicine.medical_treatment, T-Lymphocytes, Breast Neoplasms, microfluidic chip, chemotherapy, Polymorphism, Single Nucleotide, Formyl peptide receptor 1, immune response, Mice, Immune system, Immunity, Cell Line, Tumor, Neoplasms, medicine, Leukocytes, Animals, Humans, Anthracyclines, Alleles, Annexin A1, Chemotherapy, Multidisciplinary, business.industry, Dendritic Cells, medicine.disease, Receptors, Formyl Peptide, Immunity, Innate, Chemotherapy, Adjuvant, Cancer cell, Immunology, Cancer research, Female, business, Colorectal Neoplasms, Adjuvant, FPR1 microfluidic
Abstract

How dying tumor cells get noticed Besides killing tumor cells directly, some chemotherapies, such as anthracyclines, also activate the immune system to kill tumors. Vacchelli et al. discovered that in mice, anthracycline-induced antitumor immunity requires immune cells to express the protein formyl peptide receptor 1 (FPR1). Dendritic cells (DCs) near tumors expressed especially high amounts of FPR1. DCs normally capture fragments of dying tumor cells and use them to activate nearby T cells to kill tumors, but DCs lacking FPR1 failed to do this effectively. Individuals with breast or colon cancer expressing a variant of FPR1 and treated with anthracyclines showed poor metastasis-free and overall survival. Thus, FPR1 may affect anti-tumor immunity in people, too. Science , this issue p. 972

Published
2015

4. CCL2/CCR2-Dependent Recruitment of Functional Antigen-Presenting Cells into Tumors upon Chemotherapy.

Author

Yuting Ma, Mattarollo, Stephen R., Adjemian, Sandy, Heng Yang, Aymeric, Laetitia, Hannani, Dalil, Catani, João Paulo Portela, Duret, Helene, Teng, Michele W. L., Kepp, Oliver, Yidan Wang, Sistigu, Antonella, Schultze, Joachim L., Stoll, Gautier, Galluzzi, Lorenzo, Zitvogel, Laurence, Smyth, Mark J., and Kroemer, Guido

Subjects
*ANTHRACYCLINES, *DENDRITIC cells, *TUMOR growth, *CANCER chemotherapy, *IMMUNOREGULATION
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+Ly6ChighLy6G-MHCII+ dendritic cell--like antigenpresenting 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. [ABSTRACT FROM AUTHOR]

Published
2014
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5. Tumor necrosis factor is dispensable for the success of immunogenic anticancer chemotherapy.

Author

Yuting Ma, Yamazaki, Takahiro, Heng Yang, Kepp, Oliver, Galluzzi, Lorenzo, Zitvogel, Laurence, Smyth, Mark J., and Kroemer, Guido

Subjects
*TUMOR necrosis factors, *IMMUNOGENETICS, *CANCER chemotherapy, *ANTINEOPLASTIC agents, *ANTHRACYCLINES, *DENDRITIC cells
Abstract

The antineoplastic effects of anthracyclines have been shown to rely, at least in part, on a local immune response that involves dendritic cells (DCs) and several distinct subsets of T lymphocytes. Here, we show that the administration of anthracyclines to mice bearing established neoplasms stimulates the intratumoral secretion of tumor necrosis factor α (TNFα). However, blocking the TNFα/TNF receptor (TNFR) system by three different strategies—namely, (1) neutralizing antibodies, (2) etanercept, a recombinant protein in which TNFR is fused to the constant domain of an IgG1 molecule, and (3) gene knockout—failed to negatively affect the therapeutic efficacy of anthracyclines in three distinct tumor models. In particular, TNFα-blocking strategies did not influence the antineoplastic effects of doxorubicin (a prototypic anthracycline) against MCA 205 fibrosarcomas growing in C57BL/6 mice, F244 sarcomas developing in 129/Sv hosts and H2N100 mammary carcinomas arising in BALB/c mice. These findings imply that, in contrast to other cytokines (such as interleukin-1β, interleukin-17 and interferon γ), TNFα is not required for anthracyclines to elicit therapeutic anticancer immune responses. [ABSTRACT FROM AUTHOR]

Published
2013
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