Zitvogel, L. (Laurence)
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- Classification of current anticancer immunotherapies(Impact Journals, 2014) Bracci, L. (Laura); Silva-Santos, B. (Bruno); Mach, J.P. (Jean-Pierre); Hoos, A. (Axel); Abastado, J.P. (Jean-Pierre); Ayyoub, M. (Maha); Whiteside, T.L. (Theresa L.); Vile, R.G. (Richard G.); Rizvi, N. (Naiyer); Galon, J. (Jerome); Odunsi, A. (Adekunke); Kirkwood, J.M. (John M.); Galluzzi, L. (Lorenzo); Ghiringhelli, F. (François); Cerundolo, V. (Vincenzo); Gabrilovich, D.I. (Dmitry I.); Melief, C.J. (Cornelis J.); Speiser, D.E. (Daniel E.); Castoldi, F. (Francesca); Kalinski, P. (Pawel); Senovilla, L. (Laura); Tartour, E. (Eric); Colombo, M.P. (Mario P.); Schreiber, H. (Hans); Jäger, D. (Dirk); Mavilio, D. (Domenico); Kroemer, G. (Guido); Apte, R.N. (Ron N.); Porgador A. (Ángel); Blay, J.Y. (Jean-Yves); Fucíková, J. (Jitka); Rabinovich, G.A. (Gabriel A.); Sautès-Fridman, C. (Catherine); Lugli, E. (Enrico); Fridman, W.H. (Wolf H.); Baracco, E.E. (Elisa Elena); Van-Der-Burg, S.H. (Sjoerd H.); Klein, E. (Eva); Srivastava, P.K. (Pramod K.); Kärre, K. (Klas); Gnjatic,S. (Sacha); Agostinis, P. (Patrizia); Aranda, F. (Fernando); Lewis, C.E. (Claire E.); Bloy, N. (Norma); Vacchelli, E. (Erika); Caignard, A. (Anne); Melero, I. (Ignacio); Kiessling, R. (Rolf); Restifo, N.P. (Nicholas P.); Smyth, M.J. (Mark J.); Zitvogel, L. (Laurence); Fearon, D.T. (Douglas T.); Seliger, B. (Barbara); Prendergast, G.C. (George C.); Pienta, K.J. (Kenneth J.); Wolchok, J.D. (Jedd D.); Clayton, A. (Aled); Cavallo, F. (Federica); Hosmalin, A. (Anne); Knuth, A. (Alexander); Lotze, M.T. (Michael T.); Coussens, L. (Lisa); Beckhove, P. (Philipp); Gilboa, E. (Eli); Mittendorf, E.A. (Elizabeth A.); Palucka, A.K. (Anna Karolina); Weber, J.S. (Jeffrey S.); Talmadge, J.E. (James E.); Celis, E. (Esteban); Castelli, C. (Chiara); Spisek, R. (Radek); Zou, W. (Weiping); Eggermont, A.M. (Alexander M.); Garg, A. (Abhishek); Okada, H. (Hideho); Buque, A. (Aitziber); Mattei, F. (Fabrizio); Bravo-San-Pedro, J.M. (José-Manuel); Moretta, L. (Lorenzo); Dhodapkar, M.V. (Madhav V.); Van-Den-Eynde, B.J. (Benoît J.); Peter, M.E. (Marcus E.); Shiku, H. (Hiroshi); Liblau, R. (Roland); Giaccone, G. (Giuseppe); Kepp, O. (Oliver); Wagner, H. (Hermann)During the past decades, anticancer immunotherapy has evolved from a promising therapeutic option to a robust clinical reality. Many immunotherapeutic regimens are now approved by the US Food and Drug Administration and the European Medicines Agency for use in cancer patients, and many others are being investigated as standalone therapeutic interventions or combined with conventional treatments in clinical studies. Immunotherapies may be subdivided into “passive” and “active” based on their ability to engage the host immune system against cancer. Since the anticancer activity of most passive immunotherapeutics (including tumor-targeting monoclonal antibodies) also relies on the host immune system, this classification does not properly reflect the complexity of the drug-host-tumor interaction. Alternatively, anticancer immunotherapeutics can be classified according to their antigen specificity. While some immunotherapies specifically target one (or a few) defined tumor-associated antigen(s), others operate in a relatively non-specific manner and boost natural or therapy-elicited anticancer immune responses of unknown and often broad specificity. Here, we propose a critical, integrated classification of anticancer immunotherapies and discuss the clinical relevance of these approaches.
- Contribution of IL-17-producing gamma delta T cells to the efficacy of anticancer chemotherapy(Rockefeller University Press, 2011) Delahaye, N.F. (Nicolas F.); Ghiringhelli, F. (François); Chaput, N. (Nathalie); Mattarollo, S.R. (Stephen R.); Tesniere, A. (Antoine); Ikuta, K. (Koichi); Kroemer, G. (Guido); Ryffel, B. (Bernard); Pereira, P. (Pablo); Casares, N. (Noelia); Matsuzaki, G. (Goro); Benlagha, K. (Kamel); Apetoh, L. (Lionel); Smyth, M.J. (Mark J.); Zitvogel, L. (Laurence); Ma, Y. (Yuting); Dechanet-Mervill, J. (Julie); Boucontet, L. (Laurent); Ibrahim, N. (Nicolás); Locher, C. (Clara); Aymeric, L. (Laetitia); Lasarte, J.J. (Juan José)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.
- Defining the Critical Hurdles in Cancer Immunotherapy(Biomed Central, 2011) Kotlan, B. (Beatrix); Ottensmeier, C. (Christian); Zwierzina, H. (Heinz); Butterfield, L.H. (Lisa H.); Nelief, C. (Cornelious); Gajewski, T.F. (Thomas F.); Borden, E. (Ernest); Bonorino, C. C. (Cristina C.); Song, W. (Wenru); Hoos, A. (Axel); Grizzi, F. (Fabio); Characiejus, D. (Dainius); Galon, J. (Jerome); Kaufman, H.L. (Howard L.); Coukos, G. (George); Kawakami, K. (Koji); Dillman, R.O. (Robert O.); Ribas, A. (Antoni); Herberman, R.B. (Ronald B.); Kalinski, P. (Pawel); Durrant, L.G. (Lindy G.); Hwu, P. (Patrick); Aamdal, S. (Steinar); Straten, P.T. (Per Thor); Wang, E. (Ena); Finke, J.H. (James H.); Romero, P.J. (Pedro J.); Withington, T. (Tara); Schendel, D. J. (Dolores J.); Scheper, R.J. (Rik J.); Disis, M.L. (Mary L.); Old, LL.J. (LLoyd J.); Allison, J.P. (James P.); Singh-Jasuja, H. (Harpreet); Kroemer, G. (Guido); Guida, M. (Michele); Dranoff, G. (Glenn); Kawakami, Y. (Yutaka); Hodi, F.S. (F. Stephen); Jaffee, E.M. (Elizabeth M.); Maio, M. (Michele); Maccalli, C. (Cristina); Salem, M.L. (Mohamed L.); Van-Der-Burg, S.H. (Sjoerd H.); Gollob, J.A. (Jared A.); Khleif, S.N. (Samir N.); Bergmann, L. (Lothar); Wigginton, J.M. (Jon M.); Xiao, W. (Weihua); Qin, S. (Shukui); Bartunkova, J. (Jirina); Britten, C.M. (Cedrik M.); Nelson, B. (Brad); Berinstein, N. (Neil); Rivoltini, L. (Licia); Proietti, E. (Enrico); Melero, I. (Ignacio); Mastrangelo, M.J. (Michael J.); Kiessling, R. (Rolf); Chang, A.E. (Alfred E.); Keilholtz, U. (Ulrich); Parmiani, G. (Giorgio); Janetzki, S. (Sylvia); Zitvogel, L. (Laurence); Seliger, B. (Barbara); Rees, R. (Robert); O'Donnell-Tormey, J. (Jill); Levitsky, H.I. (Hyam I.); Hakansson, L. (Leif); Nishimura, M.I. (Michael I.); Marschner, J-P. (Jens-Peter); Wolchok, J.D. (Jedd D.); Ohashi, P.S. (Pamela S.); Sharma, P. (Padmanee); Imai, K. (Kohzoh); Winter, H. (Hauke); Ritter, G. (Gerd); Odunsi, K. (Kunle); Fox, B.A. (Bernard A.); Von Hoegen, P. (Paul); Gruijl, T. (Tanja); Nicolini, A. (Andrea); Welters, M. J. (Maris J.); Hege, K. (Kristen); Lotze, M.T. (Michael T.); Murphy, W.J. (William J.); Atkins, M.B. (Michael B.); Dolstra, H. (Harry); Lapointe, R. (Rejean); Masucci, G. (Giuseppe); Cao, X. (Xuetao); Tian, Z. (Zigang); Ascierto, P.A. (Paolo Antonio); Huber, C. (Christoph); Tahara, H. (Hideaki); Pawelec, G. (Graham); June, C.H. (Carl H.); Carson, W.E. (William E.); Papamichail, M. (Michael); Choudhury, A.R. (A. Raja); Marincola, F.M. (Francesco M.); Shiku, H. (Hiroshi); Bramson, J.L. (Jonathan L.); Ridolfi, R. (Ruggero); Gouttefangeas, C. (Cecile)ABSTRACT: Scientific discoveries that provide strong evidence of antitumor effects in preclinical models often encounter significant delays before being tested in patients with cancer. While some of these delays have a scientific basis, others do not. We need to do better. Innovative strategies need to move into early stage clinical trials as quickly as it is safe, and if successful, these therapies should efficiently obtain regulatory approval and widespread clinical application. In late 2009 and 2010 the Society for Immunotherapy of Cancer (SITC), convened an "Immunotherapy Summit" with representatives from immunotherapy organizations representing Europe, Japan, China and North America to discuss collaborations to improve development and delivery of cancer immunotherapy. One of the concepts raised by SITC and defined as critical by all parties was the need to identify hurdles that impede effective translation of cancer immunotherapy. With consensus on these hurdles, international working groups could be developed to make recommendations vetted by the participating organizations. These recommendations could then be considered by regulatory bodies, governmental and private funding agencies, pharmaceutical companies and academic institutions to facilitate changes necessary to accelerate clinical translation of novel immune-based cancer therapies. The critical hurdles identified by representatives of the collaborating organizations, now organized as the World Immunotherapy Council, are presented and discussed in this report. Some of the identified hurdles impede all investigators, others hinder investigators only in certain regions or institutions or are more relevant to specific types of immunotherapy or first-in-humans studies. Each of these hurdles can significantly delay clinical translation of promising advances in immunotherapy yet be overcome to improve outcomes of patients with cancer.
- Consensus guidelines for the definition, detection and interpretation of immunogenic cell death(Bmj, 2020) Hemmink, A. (Akseli); Gaipl, U.S. (Udo S.); Draganov, D. (Dobrin); Karin, M. (Michael); Mossman, K.L. (Karen L.); Zamarin, D. (Dmitriy); Gool, S.W. (Stefaan W.) van; Kaufman, H.L. (Howard L.); Galluzzi, L. (Lorenzo); Coukos, G. (George); Tang, D. (Daolin); Cesano, A. (Alessandra); Melcher, A. (Alan); Kroemer, G. (Guido); Riganti, C. (Chiara); Han, J. (Jian); Sistigu, A. (Antonella); Tatsuno, K. (Kazuko); Merghoub, T. (Taha); Buqué-Martinez, A. (Aitziber); Rescigno, M. (Maria); Rekdal, O. (Oystein); Loi, S. (Sherene); Fucíková, J. (Jitka); Manic, G. (Gwenola); Strauss, B.E. (Bryan E.); Harrington, K. (K.); Gameiro, S.R. (Sofa R.); Stagg, J. (John); Agostinis, P. (Patrizia); Illidge, T. (Tim); Warren, S. (Sarah); Vandenabeele, P. (Peter); Adjemian, S. (Sandy); Smyth, M.J. (Mark J.); Zitvogel, L. (Laurence); Chan, T.A. (Timothy A.); Yamazaki, T. (Takahiro); Demaria, S. (Sandra); Hodge, J.W. (James W.); Lotze, M.T. (Michael T.); Edelson, R.L. (Richard L.); Vitale, I. (Ilio); Prosper-Cardoso, F. (Felipe); Spisek, R. (Radek); Garg, A. (Abhishek); Golden, E. (Encouse); Sakib-Hossain, D. (Dewan); Formenti, S.C. (Silvia C.); Marincola, F.M. (Francesco M.); Kepp, O. (Oliver); Deutsch, É. (Éric); Gabriele, L. (Lucia); Lasarte, J.J. (Juan José)Cells succumbing to stress via regulated cell death (RCD) can initiate an adaptive immune response associated with immunological memory, provided they display sufficient antigenicity and adjuvanticity. Moreover, multiple intracellular and microenvironmental features determine the propensity of RCD to drive adaptive immunity. Here, we provide an updated operational definition of immunogenic cell death (ICD), discuss the key factors that dictate the ability of dying cells to drive an adaptive immune response, summarize experimental assays that are currently available for the assessment of ICD in vitro and in vivo, and formulate guidelines for their interpretation.