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Statements

Subject Item
n2:RIV%2F00216208%3A11130%2F14%3A10293140%21RIV15-MSM-11130___
rdf:type
skos:Concept n14:Vysledek
rdfs:seeAlso
http://dx.doi.org/10.4161/21624011.2014.955691
dcterms:description
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 %22immunogenic cell death%22 (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. 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 %22immunogenic cell death%22 (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.
dcterms:title
Consensus guidelines for the detection of immunogenic cell death Consensus guidelines for the detection of immunogenic cell death
skos:prefLabel
Consensus guidelines for the detection of immunogenic cell death Consensus guidelines for the detection of immunogenic cell death
skos:notation
RIV/00216208:11130/14:10293140!RIV15-MSM-11130___
n3:aktivita
n11:I
n3:aktivity
I
n3:cisloPeriodika
9
n3:dodaniDat
n15:2015
n3:domaciTvurceVysledku
n5:1110047 n5:8086478
n3:druhVysledku
n19:J
n3:duvernostUdaju
n18:S
n3:entitaPredkladatele
n7:predkladatel
n3:idSjednocenehoVysledku
8637
n3:idVysledku
RIV/00216208:11130/14:10293140
n3:jazykVysledku
n13:eng
n3:klicovaSlova
immunotherapy; HMGB1; endoplasmic reticulum stress; calreticulin; autophagy; ATP release
n3:klicoveSlovo
n4:immunotherapy n4:calreticulin n4:endoplasmic%20reticulum%20stress n4:autophagy n4:ATP%20release n4:HMGB1
n3:kodStatuVydavatele
US - Spojené státy americké
n3:kontrolniKodProRIV
[C8DF6D09929F]
n3:nazevZdroje
OncoImmunology
n3:obor
n10:EC
n3:pocetDomacichTvurcuVysledku
2
n3:pocetTvurcuVysledku
82
n3:rokUplatneniVysledku
n15:2014
n3:svazekPeriodika
3
n3:tvurceVysledku
Dini, Luciana Ma, Yuting Cremer, Isabelle Bloy, Norma Aranda, Fernando Illidge, Tim M. Hodge, James W. Gabriele, Lucia Adjemian, Sandy Cirone, Mara Lowenstein, Pedro R. Senovilla, Laura Kepp, Oliver … Giese, Nathalia A. Oehler, Rudolf Manfredi, Angelo A. Apetoh, Lionel Martins, Isabelle Colombo, Maria I. Mossman, Karen L. Loi, Sherene Lugli, Enrico Agostinis, Patrizia Krysko, Dmitri V. Madeo, Frank Barnaba, Vincenzo Vacchelli, Erika Garg, Abhishek Breckpot, Karine Korbelik, Mladen Vitale, Ilio Faggioni, Alberto Michaud, Michael Bracci, Laura Kono, Koji Gaipl, Udo S. Eliopoulos, Aristides G. Buque, Aitziber Guo, Zong Sheng Formenti, Silvia C. Menger, Laurie Mignot, Gregoire Mavilio, Domenico Galon, Jerome Herrmann, Martin Brough, David Castro, Maria G. Ghiringhelli, Francois Huang, Xing Demaria, Sandra Honeychurch, Jamie Holdenrieder, Stefan Fučíková, Jitka Hemminki, Akseli Multhoff, Gabriele Hu, Hong-Min Merendino, Nicolo
n3:wos
000346922400019
s:issn
2162-4011
s:numberOfPages
19
n8:doi
10.4161/21624011.2014.955691
n17:organizacniJednotka
11130