10 results on '"Galluzzi, Lorenzo"'
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2. ATP and cancer immunosurveillance.
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Kepp, Oliver, Bezu, Lucillia, Yamazaki, Takahiro, Di Virgilio, Francesco, Smyth, Mark J, Kroemer, Guido, and Galluzzi, Lorenzo
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ADENOSINE triphosphate ,CELL receptors ,TUMOR microenvironment ,IMMUNE checkpoint inhibitors ,PURINERGIC receptors ,METABOLITES - Abstract
While intracellular adenosine triphosphate (ATP) occupies a key position in the bioenergetic metabolism of all the cellular compartments that form the tumor microenvironment (TME), extracellular ATP operates as a potent signal transducer. The net effects of purinergic signaling on the biology of the TME depend not only on the specific receptors and cell types involved, but also on the activation status of cis‐ and trans‐regulatory circuitries. As an additional layer of complexity, extracellular ATP is rapidly catabolized by ectonucleotidases, culminating in the accumulation of metabolites that mediate distinct biological effects. Here, we discuss the molecular and cellular mechanisms through which ATP and its degradation products influence cancer immunosurveillance, with a focus on therapeutically targetable circuitries. [ABSTRACT FROM AUTHOR]
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- 2021
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3. Detection of Apoptotic Versus Autophagic Cell Death by Flow Cytometry
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Sica, Valentina, Kroemer, Guido, Galluzzi, Lorenzo, MAIURI, MARIA CHIARA, Sica, Valentina, Maiuri, MARIA CHIARA, Kroemer, Guido, and Galluzzi, Lorenzo
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Mitochondrial permeability transition ,Necroptosi ,Necrosis ,Mitochondrial outer membrane permeabilization ,Autophagy ,Immunogenic cell death - Abstract
Different modes of regulated cell death (RCD) can be initiated by distinct molecular machineries and their morphological manifestations can be difficult to discriminate. Moreover, cells responding to stress often activate an adaptive response centered around autophagy, and whether such a response is cytoprotective or cytotoxic cannot be predicted based on morphological parameters only. Molecular definitions are therefore important to understand various RCD subroutines from a mechanistic perspective. In vitro, various forms of RCD including apoptosis and autophagic cell death can be easily discriminated from each other with assays that involve chemical or pharmacological interventions targeting key components of either pathway. Here, we detail a straightforward method to discriminate apoptosis from autophagic cell death by flow cytometry, based on the broad-spectrum caspase inhibitor Z-VAD-fmk and the genetic inhibition of ATG5.
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- 2016
4. Mitochondrial control of innate immune signaling by irradiated cancer cells.
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Yamazaki, Takahiro and Galluzzi, Lorenzo
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CANCER cells , *TYPE I interferons , *MITOCHONDRIA , *MITOCHONDRIAL DNA , *MITOCHONDRIAL membranes - Abstract
Type I interferon (IFN) release by irradiated cancer cells is paramount for radiation therapy to elicit anticancer immunity. Our findings demonstrate that mitochondrial outer membrane permeabilization (MOMP) triggered by RT enables exposure of mitochondrial DNA to the cytosol, hence setting off CGAS-driven type I IFN synthesis. These data point to the existence of a therapeutically actionable mitochondrial checkpoint that restricts innate immune signaling in irradiated cancer cells. [ABSTRACT FROM AUTHOR]
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- 2020
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5. Combinatorial Strategies for the Induction of Immunogenic Cell Death
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Bezu, Lucillia, Gomes-de-Silva, Ligia C., Dewitte, Heleen, Breckpot, Karine, Fucikova, Jitka, Spisek, Radek, Galluzzi, Lorenzo, Kepp, Oliver, Kroemer, Guido, Apoptose, cancer et immunité (Equipe labellisée Ligue contre le cancer - CRC - Inserm U1138), Institut Gustave Roussy (IGR)-Centre de Recherche des Cordeliers (CRC), 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), Université Paris-Sud - Paris 11 - Faculté de médecine (UP11 UFR Médecine), Université Paris-Sud - Paris 11 (UP11), Centre de Recherche des Cordeliers (CRC), Plateforme de métabolomique, Direction de la recherche [Gustave Roussy], Institut Gustave Roussy (IGR)-Institut Gustave Roussy (IGR), Department of Chemistry, University of Coimbra, Universiteit Gent = Ghent University (UGENT), Vrije Universiteit Brussel (VUB), Dept. of Immunology, 2nd Faculty of Medicine and University Hospital Motol, Charles University [Prague] (CU), Sotio a.c., Institut Gustave Roussy (IGR), Université Paris Descartes - Paris 5 (UPD5), Université Pierre et Marie Curie - Paris 6 (UPMC), Pôle de biologie, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Européen Georges Pompidou [APHP] (HEGP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO), Laboratory of Molecullar and Cellular Therapy, Basic (bio-) Medical Sciences, 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), HAL-UPMC, Gestionnaire, Apoptose, cancer et immunité ( Equipe labellisée Ligue contre le cancer - CRC - Inserm U1138 ), Institut Gustave Roussy ( IGR ) -Centre de Recherche des Cordeliers ( CRC ), 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 Paris-Sud 11 - Faculté de médecine ( UP11 UFR Médecine ), Centre de Recherche des Cordeliers ( CRC ), 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 ), Institut Gustave Roussy ( IGR ) -Institut Gustave Roussy ( IGR ), Ghent University [Belgium] ( UGENT ), Vrije Universiteit [Brussel] ( VUB ), Charles University, Institut Gustave Roussy ( IGR ), Université Paris Descartes - Paris 5 ( UPD5 ), Université Pierre et Marie Curie - Paris 6 ( UPMC ), Assistance publique - Hôpitaux de Paris (AP-HP)-Hôpital Européen Georges Pompidou [APHP] ( HEGP ), 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), and Universiteit Gent = Ghent University [Belgium] (UGENT)
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CANCER-THERAPY ,autophagy ,ANTICANCER IMMUNE-RESPONSES ,Immunology ,CHEMOTHERAPEUTIC-AGENTS ,SURFACE EXPRESSION ,[SDV.BC]Life Sciences [q-bio]/Cellular Biology ,Review ,IFN ,calreticulin ,immunogenic cell death ,Medicine and Health Sciences ,Immunology and Allergy ,HUMAN TUMOR-CELLS ,ATP SECRETION ,[SDV.BC] Life Sciences [q-bio]/Cellular Biology ,HMGB1 ,CALRETICULIN EXPOSURE ,MOLECULAR-MECHANISMS ,[ SDV.BC ] Life Sciences [q-bio]/Cellular Biology ,General Commentary ,ER STRESS ,ATP ,endoplasmic reticulum stress ,type I interferon ,HMGB1 protein - Abstract
International audience; The term “immunogenic cell death” (ICD) is commonly employed to indicate a peculiar instance of regulated cell death (RCD) that engages the adaptive arm of the immune system. The inoculation of cancer cells undergoing ICD into immunocompetent animals elicits a specific immune response associated with the establishment of immunological memory. Only a few agents are intrinsically endowed with the ability to trigger ICD. These include a few chemotherapeutics that are routinely employed in the clinic, like doxorubicin, mitoxantrone, oxaliplatin, and cyclophosphamide, as well as some agents that have not yet been approved for use in humans. Accumulating clinical data indicate that the activation of adaptive immune responses against dying cancer cells is associated with improved disease outcome in patients affected by various neoplasms. Thus, novel therapeutic regimens that trigger ICD are urgently awaited. Here, we discuss current combinatorial approaches to convert otherwise non-immunogenic instances of RCD into bona fide ICD.
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- 2015
6. Immune recognition of irradiated cancer cells.
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Wennerberg, Erik, Vanpouille-Box, Claire, Bornstein, Sophia, Yamazaki, Takahiro, Demaria, Sandra, and Galluzzi, Lorenzo
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CANCER cells ,IMMUNE recognition ,IONIZING radiation ,PALLIATIVE treatment ,CANCER radiotherapy - Abstract
Ionizing irradiation has been extensively employed for the clinical management of solid tumors, with therapeutic or palliative intents, for decades. Until recently, radiation therapy ( RT) was believed to mediate antineoplastic activity mostly (if not only) as a consequence of cancer cell-intrinsic effects. Indeed, the macromolecular damage imposed to malignant cells by RT initiates one or multiple signal transduction cascades that drive a permanent proliferative arrest (cellular senescence) or regulated cell death. Both these phenomena show a rather linear dose-response correlation. However, RT also mediates consistent immunological activity, not only as an 'on-target effect' originating within irradiated cancer cells, but also as an 'off-target effect' depending on the interaction between RT and stromal, endothelial, and immune components of the tumor microenvironment. Interestingly, the immunological activity of RT does not exhibit linear dose-response correlation. Here, we discuss the mechanisms whereby RT alters the capacity of the immune system to recognize and eliminate irradiated cancer cells, either as an 'on-target' or as on 'off-target' effect. In particular, we discuss the antagonism between the immunostimulatory and immunosuppressive effects of RT as we delineate combinatorial strategies to boost the former at the expenses of the latter. [ABSTRACT FROM AUTHOR]
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- 2017
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7. Immunogenic cell death in radiation therapy.
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Galluzzi, Lorenzo, Kepp, Oliver, and Kroemer, Guido
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RADIOTHERAPY , *CELL death , *AUTOPHAGY , *TUMOR treatment , *NUCLEOTIDASES , *IMMUNOGENETICS , *ANTINEOPLASTIC agents - Abstract
The author presents information on immunogenic cell death in radiation therapy. He discusses the antineoplastic effects of radiation therapy, and mentions about the cancer cell-intrinsic and extrinsic mechanism. He also discusses the radiotherapy of autophagy-incompetent tumors along with pharmacological inhibition of extracellular nucleotidases.
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- 2013
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8. ATP-dependent recruitment, survival and differentiation of dendritic cell precursors in the tumor bed after anticancer chemotherapy.
- Author
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Yuting Ma, Adjemian, Sandy, Heng Yang, Portela Catani, João Paulo, Hannani, Dalil, Martins, Isabelle, Michaud, Mickaël, Kepp, Oliver, Qader Sukkurwala, Abdul, Vacchelli, Erika, Galluzzi, Lorenzo, Zitvogel, Laurence, and Kroemer, Guido
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ADENOSINE triphosphate ,DENDRITIC cells ,CANCER chemotherapy ,TUMOR antigens ,EXTRACELLULAR enzymes - Abstract
Tumor cells succumb to chemotherapy while releasing ATP. We have found that extracellular ATP attracts dendritic cell (DC) precursors into the tumor bed, facilitates their permanence in the proximity of dying cells and promotes their differentiation into mature DCs endowed with the capacity of presenting tumor-associated antigens. [ABSTRACT FROM AUTHOR]
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- 2013
- Full Text
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9. Chemokines and chemokine receptors required for optimal responses to anticancer chemotherapy.
- Author
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Ma, Yuting, Adjemian, Sandy, Galluzzi, Lorenzo, Zitvogel, Laurence, and Kroemer, Guido
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CHEMOKINES ,CHEMOKINE receptors ,CANCER chemotherapy ,DISEASE progression ,LIGANDS (Biochemistry) ,CANCER invasiveness ,T cells - Abstract
Depending on tumor type, stage and immunological contexture, the inhibition of chemokines or their receptors may yield positive or deleterious effects on disease progression. We have recently demonstrated in several murine models of anthracycline-based chemotherapy that the inhibition of chemokine (C-C motif) ligand 2 (CCL2) or chemokine (C-C motif) receptor 2 (CCR2) may impair the elicitation of anticancer immune responses that contribute to therapeutic success. [ABSTRACT FROM PUBLISHER]
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- 2014
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10. Consensus guidelines for the detection of immunogenic cell death
- Author
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Kepp, O., Senovilla, L., Vitale, I., Vacchelli, E., Adjemian, S., Agostinis, P., Apetoh, L., Aranda, F., Barnaba, V., Bloy, N., Bracci, L., Breckpot, K., Brough, D., Buqué, A., Castro, Mg, Cirone, M., Colombo, Mi, Cremer, I., Demaria, S., Dini, L., Eliopoulos, A., Faggioni, A., Formenti, Sc, Fu??íková, J., Gabriele, L., Gaipl, Us, Galon, J., Garg, A., Ghiringhelli, F., Giese, Na, Guo, Zs, Hemminki, A., Herrmann, M., Hodge, Jw, Holdenrieder, S., Honeychurch, J., Hm, Hu, Huang, X., Illidge, Tm, Kono, K., Korbelik, M., Krysko, Dv, Loi, S., Lowenstein, Pr, Lugli, E., Ma, Y., Madeo, F., Manfredi, Aa, Martins, I., Matzinger, P., Mavilio, D., Menger, L., Merendino, N., Michaud, M., Mignot, G., Mossman, Kl, Multhoff, G., Oehler, R., Palombo, F., Panaretakis, T., Pol, J., Proietti, E., Ricci, Je, Riganti, Chiara, Rovere Querini, P., Rubartelli, A., Sistigu, A., Smyth, Mj, Sonnemann, J., Spisek, R., Stagg, J., Sukkurwala, Aq, Tartour, E., Thorburn, A., Thorne, Sh, Vandenabeele, P., Velotti, F., Workenhe, Sr, Yang, H., Zong, Wx, Zitvogel, L., Kroemer, G., Galluzzi, L., Medicine and Pharmacy academic/administration, Basic (bio-) Medical Sciences, Laboratory of Molecullar and Cellular Therapy, Chemistry, Kepp, Oliver, Senovilla, Laura, Vitale, Ilio, Vacchelli, Erika, Adjemian, Sandy, Agostinis, Patrizia, Apetoh, Lionel, Aranda, Fernando, Barnaba, Vincenzo, Bloy, Norma, Bracci, Laura, Breckpot, Karine, Brough, David, Buqué, Aitziber, Castro, Maria G, Cirone, Mara, Colombo, Maria I, Cremer, Isabelle, Demaria, Sandra, Dini, Luciana, Eliopoulos, Aristides G, Faggioni, Alberto, Formenti, Silvia C, Fučíková, Jitka, Gabriele, Lucia, Gaipl, Udo S, Galon, Jérôme, Garg, Abhishek, Ghiringhelli, Françoi, Giese, Nathalia A, Guo, Zong Sheng, Hemminki, Akseli, Herrmann, Martin, Hodge, James W, Holdenrieder, Stefan, Honeychurch, Jamie, Hu, Hong Min, Huang, Xing, Illidge, Tim M, Kono, Koji, Korbelik, Mladen, Krysko, Dmitri V, Loi, Sherene, Lowenstein, Pedro R, Lugli, Enrico, Ma, Yuting, Madeo, Frank, Manfredi, Angelo A, Martins, Isabelle, Mavilio, Domenico, Menger, Laurie, Merendino, Nicolò, Michaud, Michael, Mignot, Gregoire, Mossman, Karen L, Multhoff, Gabriele, Oehler, Rudolf, Palombo, Fabio, Panaretakis, Theochari, Pol, Jonathan, Proietti, Enrico, Ricci, Jean Ehrland, Riganti, Chiara, Rovere Querini, Patrizia, Rubartelli, Anna, Sistigu, Antonella, Smyth, Mark J, Sonnemann, Juergen, Spisek, Radek, Stagg, John, Sukkurwala, Abdul Qader, Tartour, Eric, Thorburn, Andrew, Thorne, Stephen H, Vandenabeele, Peter, Velotti, Francesca, Workenhe, Samuel T, Yang, Haining, Zong, Wei Xing, Zitvogel, Laurence, Kroemer, Guido, Galluzzi, Lorenzo, Kepp, O, Senovilla, L, Vitale, I, Vacchelli, E, Adjemian, S, Agostinis, P, Apetoh, L, Aranda, F, Barnaba, V, Bloy, N, Bracci, L, Breckpot, K, Brough, D, Buque, A, Castro, Mg, Cirone, M, Colombo, Mi, Cremer, I, Demaria, S, Dini, L, Eliopoulos, Ag, Faggioni, A, Formenti, Sc, Fucikova, J, Gabriele, L, Gaipl, U, Galon, J, Garg, A, Ghiringhelli, F, Giese, Na, Guo, Z, Hemminki, A, Herrmann, M, Hodge, Jw, Holdenrieder, S, Honeychurch, J, Hu, Hm, Huang, X, Illidge, Tm, Kono, K, Korbelik, M, Krysko, Dv, Loi, S, Lowenstein, Pr, Lugli, E, Ma, Yt, Madeo, F, Manfredi, ANGELO ANDREA M. A., Martins, I, Mavilio, D, Menger, L, Merendino, N, Michaud, M, Mignot, G, Mossman, Kl, Multhoff, G, Oehler, R, Palombo, F, Panaretakis, T, Pol, J, Proietti, E, Ricci, Je, Riganti, C, ROVERE QUERINI, Patrizia, Rubartelli, A, Sistigu, A, Smyth, Mj, Sonnemann, J, Spisek, R, Stagg, J, Sukkurwala, Aq, Tartour, E, Thorburn, A, Thorne, Sh, Vandenabeele, P, Velotti, F, Workenhe, St, Yang, Hn, Zong, Wx, Zitvogel, L, Kroemer, G, and Galluzzi, L.
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HSV-1, herpes simplex virus type I ,Δψm, mitochondrial transmembrane potential ,medicine.medical_treatment ,DAMP, damage-associated molecular pattern ,detection ,FLT3LG, fms-related tyrosine kinase 3 ligand ,Review ,member 3 ,calreticulin ,Eukaryotic translation initiation factor 2A ,RFP, red fluorescent protein ,0302 clinical medicine ,MOMP, mitochondrial outer membrane permeabilization ,Immunology and Allergy ,GFP, green fluorescent protein ,HMGB1 ,0303 health sciences ,education.field_of_study ,Toll-like receptor ,BAK1, BCL2-antagonist/killer 1 ,H2B, histone 2B ,endoplasmic reticulum stre ,3. Good health ,BAX, BCL2-associated X protein ,XBP1, X-box binding protein 1 ,cell death ,Oncology ,PDIA3, protein disulfide isomerase family A ,030220 oncology & carcinogenesis ,endoplasmic reticulum stress ,Immunogenic cell death ,HSP, heat shock protein ,immunotherapy ,TLR, Toll-like receptor ,autophagy ,ATF6, activating transcription factor 6 ,Immunology ,ICD, immunogenic cell death ,EIF2A, eukaryotic translation initiation factor 2A ,Guidelines ,Biology ,BCL2, B-cell CLL/lymphoma 2 protein ,ER, endoplasmic reticulum ,PI, propidium iodide ,ATP release ,03 medical and health sciences ,Immune system ,immunogenic ,medicine ,IFN, interferon ,Antigen-presenting cell ,education ,030304 developmental biology ,CALR, calreticulin ,Damage-associated molecular pattern ,Immunotherapy ,CTL, cytotoxic T lymphocyte ,HMGB1, high mobility group box 1 ,IL, interleukin ,G3BP1, GTPase activating protein (SH3 domain) binding protein 1 ,APC, antigen-presenting cell ,Cancer cell ,DiOC6(3), 3,3′-dihexyloxacarbocyanine iodide ,DAPI, 4′,6-diamidino-2-phenylindole - Abstract
Apoptotic cells have long been considered as intrinsically tolerogenic or unable to elicit immune responses specific for dead cell-associated antigens. However, multiple stimuli can trigger a functionally peculiar type of apoptotic demise that does not go unnoticed by the adaptive arm of the immune system, which we named "immunogenic cell death" (ICD). ICD is preceded or accompanied by the emission of a series of immunostimulatory damage-associated molecular patterns (DAMPs) in a precise spatiotemporal configuration. Several anticancer agents that have been successfully employed in the clinic for decades, including various chemotherapeutics and radiotherapy, can elicit ICD. Moreover, defects in the components that underlie the capacity of the immune system to perceive cell death as immunogenic negatively influence disease outcome among cancer patients treated with ICD inducers. Thus, ICD has profound clinical and therapeutic implications. Unfortunately, the gold-standard approach to detect ICD relies on vaccination experiments involving immunocompetent murine models and syngeneic cancer cells, an approach that is incompatible with large screening campaigns. Here, we outline strategies conceived to detect surrogate markers of ICD in vitro and to screen large chemical libraries for putative ICD inducers, based on a high-content, high-throughput platform that we recently developed. Such a platform allows for the detection of multiple DAMPs, like cell surface-exposed calreticulin, extracellular ATP and high mobility group box 1 (HMGB1), and/or the processes that underlie their emission, such as endoplasmic reticulum stress, autophagy and necrotic plasma membrane permeabilization. We surmise that this technology will facilitate the development of next-generation anticancer regimens, which kill malignant cells and simultaneously convert them into a cancer-specific therapeutic vaccine. peerreview_statement: The publishing and review policy for this title is described in its Aims & Scope. aims_and_scope_url: http://www.tandfonline.com/action/journalInformation?show=aimsScope&journalCode=koni20 ispartof: OncoImmunology vol:3 issue:9 pages:12472-124508 ispartof: location:United States status: published
- Published
- 2014
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