IRE1α–XBP1 controls T cell function in ovarian cancer by regulating mitochondrial activity

Autores: Song, Minkyung; Sandoval, Tito A.; Chae, Chang-Suk; Chopra, Sahil; Tan, Chen; Rutkowski, Melanie R.; Raundhal, Mahesh; Chaurio, Ricardo A.; Payne, Kyle K.; Konrad, Csaba; Bettigole, Sarah E.; Shin, Hee Rae; Crowley, Michael J. P.; Cerliani, Juan Pablo; Kossenkov, Andrew V.; Motorykin, Ievgen; Zhang, Sheng; Manfredi, Giovanni; Zamarin, Dmitriy; Holcomb, Kevin; Rodriguez, Paulo C.; Rabinovich, Gabriel Adrián; Conejo Garcia, Jose R.; Glimcher, Laurie H.; Cubillos-Ruiz, Juan R.
Año de publicación: 2018
Idioma: inglés
Tipo de recurso: artículo
Estado: versión publicada
Descripción: Tumours evade immune control by creating hostile microenvironments that perturb T cell metabolism and effector function 1?4 . However, it remains unclear how intra-tumoral T cells integrate and interpret metabolic stress signals. Here we report that ovarian cancer?an aggressive malignancy that is refractory to standard treatments and current immunotherapies 5?8 ?induces endoplasmic reticulum stress and activates the IRE1α?XBP1 arm of the unfolded protein response 9,10 in T cells to control their mitochondrial respiration and anti-tumour function. In T cells isolated from specimens collected from patients with ovarian cancer, upregulation of XBP1 was associated with decreased infiltration of T cells into tumours and with reduced IFNG mRNA expression. Malignant ascites fluid obtained from patients with ovarian cancer inhibited glucose uptake and caused N-linked protein glycosylation defects in T cells, which triggered IRE1α?XBP1 activation that suppressed mitochondrial activity and IFNγ production. Mechanistically, induction of XBP1 regulated the abundance of glutamine carriers and thus limited the influx of glutamine that is necessary to sustain mitochondrial respiration in T cells under glucose-deprived conditions. Restoring N-linked protein glycosylation, abrogating IRE1α?XBP1 activation or enforcing expression of glutamine transporters enhanced mitochondrial respiration in human T cells exposed to ovarian cancer ascites. XBP1-deficient T cells in the metastatic ovarian cancer milieu exhibited global transcriptional reprogramming and improved effector capacity. Accordingly, mice that bear ovarian cancer and lack XBP1 selectively in T cells demonstrate superior anti-tumour immunity, delayed malignant progression and increased overall survival. Controlling endoplasmic reticulum stress or targeting IRE1α?XBP1 signalling may help to restore the metabolic fitness and anti-tumour capacity of T cells in cancer hosts.
Fil: Song, Minkyung. Weill Cornell Medicine; Estados Unidos
Fil: Sandoval, Tito A.. Weill Cornell Medicine; Estados Unidos
Fil: Chae, Chang-Suk. Weill Cornell Medicine; Estados Unidos
Fil: Chopra, Sahil. Weill Cornell Medicine; Estados Unidos
Fil: Tan, Chen. Weill Cornell Medicine; Estados Unidos
Fil: Rutkowski, Melanie R.. University of Virginia; Estados Unidos
Fil: Raundhal, Mahesh. Dana Farber Cancer Institute; Estados Unidos. Harvard Medical School; Estados Unidos
Fil: Chaurio, Ricardo A.. H. Lee Moffitt Cancer Center & Research Institute; Estados Unidos
Fil: Payne, Kyle K.. H. Lee Moffitt Cancer Center & Research Institute; Estados Unidos
Fil: Konrad, Csaba. Weill Cornell Medicine; Estados Unidos
Fil: Bettigole, Sarah E.. Quentis Therapeutics Inc.; Estados Unidos
Fil: Shin, Hee Rae. Quentis Therapeutics Inc.; Estados Unidos
Fil: Crowley, Michael J. P.. Weill Cornell Graduate School of Medical Sciences; Estados Unidos
Fil: Cerliani, Juan Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina
Fil: Kossenkov, Andrew V.. The Wistar Institute; Estados Unidos
Fil: Motorykin, Ievgen. Weill Cornell Medicine,; Estados Unidos
Fil: Zhang, Sheng. Weill Cornell Medicine,; Estados Unidos
Fil: Manfredi, Giovanni. Weill Cornell Medicine,; Estados Unidos
Fil: Zamarin, Dmitriy. Memorial Sloan Kettering Cancer Center; Estados Unidos
Fil: Holcomb, Kevin. Weill Cornell Medicine,; Estados Unidos
Fil: Rodriguez, Paulo C.. H. Lee Moffitt Cancer Center & Research Institute; Estados Unidos
Fil: Rabinovich, Gabriel Adrián. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica; Argentina
Fil: Conejo Garcia, Jose R.. H. Lee Moffitt Cancer Center & Research Institute; Estados Unidos
Fil: Glimcher, Laurie H.. Dana Farber Cancer Institute; Estados Unidos. Harvard Medical School; Estados Unidos
Fil: Cubillos-Ruiz, Juan R.. Weill Graduate School Of Medical Sciences; Estados Unidos. Weill Graduate School Of Medical Sciences; Estados Unidos
Materia: IRE1
XBP1
T CELL
OVARIAN CANCER
Nivel de accesibilidad: acceso abierto
Condiciones de uso: https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
Institución: Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador: oai:ri.conicet.gov.ar:11336/87374

Acceder

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repository_id_str	3498
network_name_str	CONICET Digital (CONICET)
spelling	IRE1α–XBP1 controls T cell function in ovarian cancer by regulating mitochondrial activitySong, MinkyungSandoval, Tito A.Chae, Chang-SukChopra, SahilTan, ChenRutkowski, Melanie R.Raundhal, MaheshChaurio, Ricardo A.Payne, Kyle K.Konrad, CsabaBettigole, Sarah E.Shin, Hee RaeCrowley, Michael J. P.Cerliani, Juan PabloKossenkov, Andrew V.Motorykin, IevgenZhang, ShengManfredi, GiovanniZamarin, DmitriyHolcomb, KevinRodriguez, Paulo C.Rabinovich, Gabriel AdriánConejo Garcia, Jose R.Glimcher, Laurie H.Cubillos-Ruiz, Juan R.IRE1XBP1T CELLOVARIAN CANCERhttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1https://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3https://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Tumours evade immune control by creating hostile microenvironments that perturb T cell metabolism and effector function 1?4 . However, it remains unclear how intra-tumoral T cells integrate and interpret metabolic stress signals. Here we report that ovarian cancer?an aggressive malignancy that is refractory to standard treatments and current immunotherapies 5?8 ?induces endoplasmic reticulum stress and activates the IRE1α?XBP1 arm of the unfolded protein response 9,10 in T cells to control their mitochondrial respiration and anti-tumour function. In T cells isolated from specimens collected from patients with ovarian cancer, upregulation of XBP1 was associated with decreased infiltration of T cells into tumours and with reduced IFNG mRNA expression. Malignant ascites fluid obtained from patients with ovarian cancer inhibited glucose uptake and caused N-linked protein glycosylation defects in T cells, which triggered IRE1α?XBP1 activation that suppressed mitochondrial activity and IFNγ production. Mechanistically, induction of XBP1 regulated the abundance of glutamine carriers and thus limited the influx of glutamine that is necessary to sustain mitochondrial respiration in T cells under glucose-deprived conditions. Restoring N-linked protein glycosylation, abrogating IRE1α?XBP1 activation or enforcing expression of glutamine transporters enhanced mitochondrial respiration in human T cells exposed to ovarian cancer ascites. XBP1-deficient T cells in the metastatic ovarian cancer milieu exhibited global transcriptional reprogramming and improved effector capacity. Accordingly, mice that bear ovarian cancer and lack XBP1 selectively in T cells demonstrate superior anti-tumour immunity, delayed malignant progression and increased overall survival. Controlling endoplasmic reticulum stress or targeting IRE1α?XBP1 signalling may help to restore the metabolic fitness and anti-tumour capacity of T cells in cancer hosts.Fil: Song, Minkyung. Weill Cornell Medicine; Estados UnidosFil: Sandoval, Tito A.. Weill Cornell Medicine; Estados UnidosFil: Chae, Chang-Suk. Weill Cornell Medicine; Estados UnidosFil: Chopra, Sahil. Weill Cornell Medicine; Estados UnidosFil: Tan, Chen. Weill Cornell Medicine; Estados UnidosFil: Rutkowski, Melanie R.. University of Virginia; Estados UnidosFil: Raundhal, Mahesh. Dana Farber Cancer Institute; Estados Unidos. Harvard Medical School; Estados UnidosFil: Chaurio, Ricardo A.. H. Lee Moffitt Cancer Center & Research Institute; Estados UnidosFil: Payne, Kyle K.. H. Lee Moffitt Cancer Center & Research Institute; Estados UnidosFil: Konrad, Csaba. Weill Cornell Medicine; Estados UnidosFil: Bettigole, Sarah E.. Quentis Therapeutics Inc.; Estados UnidosFil: Shin, Hee Rae. Quentis Therapeutics Inc.; Estados UnidosFil: Crowley, Michael J. P.. Weill Cornell Graduate School of Medical Sciences; Estados UnidosFil: Cerliani, Juan Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Kossenkov, Andrew V.. The Wistar Institute; Estados UnidosFil: Motorykin, Ievgen. Weill Cornell Medicine,; Estados UnidosFil: Zhang, Sheng. Weill Cornell Medicine,; Estados UnidosFil: Manfredi, Giovanni. Weill Cornell Medicine,; Estados UnidosFil: Zamarin, Dmitriy. Memorial Sloan Kettering Cancer Center; Estados UnidosFil: Holcomb, Kevin. Weill Cornell Medicine,; Estados UnidosFil: Rodriguez, Paulo C.. H. Lee Moffitt Cancer Center & Research Institute; Estados UnidosFil: Rabinovich, Gabriel Adrián. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica; ArgentinaFil: Conejo Garcia, Jose R.. H. Lee Moffitt Cancer Center & Research Institute; Estados UnidosFil: Glimcher, Laurie H.. Dana Farber Cancer Institute; Estados Unidos. Harvard Medical School; Estados UnidosFil: Cubillos-Ruiz, Juan R.. Weill Graduate School Of Medical Sciences; Estados Unidos. Weill Graduate School Of Medical Sciences; Estados UnidosNature Publishing Group2018-10info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/87374Song, Minkyung; Sandoval, Tito A.; Chae, Chang-Suk; Chopra, Sahil; Tan, Chen; et al.; IRE1α–XBP1 controls T cell function in ovarian cancer by regulating mitochondrial activity; Nature Publishing Group; Nature; 562; 7727; 10-2018; 423-4280028-0836CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1038/s41586-018-0597-xinfo:eu-repo/semantics/altIdentifier/url/https://www.nature.com/articles/s41586-018-0597-xinfo:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/30305738/info:eu-repo/semantics/altIdentifier/pmid/30305738info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-15T15:06:12Zoai:ri.conicet.gov.ar:11336/87374instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-10-15 15:06:12.542CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv	IRE1α–XBP1 controls T cell function in ovarian cancer by regulating mitochondrial activity
title	IRE1α–XBP1 controls T cell function in ovarian cancer by regulating mitochondrial activity
spellingShingle	IRE1α–XBP1 controls T cell function in ovarian cancer by regulating mitochondrial activity Song, Minkyung IRE1 XBP1 T CELL OVARIAN CANCER
title_short	IRE1α–XBP1 controls T cell function in ovarian cancer by regulating mitochondrial activity
title_full	IRE1α–XBP1 controls T cell function in ovarian cancer by regulating mitochondrial activity
title_fullStr	IRE1α–XBP1 controls T cell function in ovarian cancer by regulating mitochondrial activity
title_full_unstemmed	IRE1α–XBP1 controls T cell function in ovarian cancer by regulating mitochondrial activity
title_sort	IRE1α–XBP1 controls T cell function in ovarian cancer by regulating mitochondrial activity
dc.creator.none.fl_str_mv	Song, Minkyung Sandoval, Tito A. Chae, Chang-Suk Chopra, Sahil Tan, Chen Rutkowski, Melanie R. Raundhal, Mahesh Chaurio, Ricardo A. Payne, Kyle K. Konrad, Csaba Bettigole, Sarah E. Shin, Hee Rae Crowley, Michael J. P. Cerliani, Juan Pablo Kossenkov, Andrew V. Motorykin, Ievgen Zhang, Sheng Manfredi, Giovanni Zamarin, Dmitriy Holcomb, Kevin Rodriguez, Paulo C. Rabinovich, Gabriel Adrián Conejo Garcia, Jose R. Glimcher, Laurie H. Cubillos-Ruiz, Juan R.
author	Song, Minkyung
author_facet	Song, Minkyung Sandoval, Tito A. Chae, Chang-Suk Chopra, Sahil Tan, Chen Rutkowski, Melanie R. Raundhal, Mahesh Chaurio, Ricardo A. Payne, Kyle K. Konrad, Csaba Bettigole, Sarah E. Shin, Hee Rae Crowley, Michael J. P. Cerliani, Juan Pablo Kossenkov, Andrew V. Motorykin, Ievgen Zhang, Sheng Manfredi, Giovanni Zamarin, Dmitriy Holcomb, Kevin Rodriguez, Paulo C. Rabinovich, Gabriel Adrián Conejo Garcia, Jose R. Glimcher, Laurie H. Cubillos-Ruiz, Juan R.
author_role	author
author2	Sandoval, Tito A. Chae, Chang-Suk Chopra, Sahil Tan, Chen Rutkowski, Melanie R. Raundhal, Mahesh Chaurio, Ricardo A. Payne, Kyle K. Konrad, Csaba Bettigole, Sarah E. Shin, Hee Rae Crowley, Michael J. P. Cerliani, Juan Pablo Kossenkov, Andrew V. Motorykin, Ievgen Zhang, Sheng Manfredi, Giovanni Zamarin, Dmitriy Holcomb, Kevin Rodriguez, Paulo C. Rabinovich, Gabriel Adrián Conejo Garcia, Jose R. Glimcher, Laurie H. Cubillos-Ruiz, Juan R.
author2_role	author author author author author author author author author author author author author author author author author author author author author author author author
dc.subject.none.fl_str_mv	IRE1 XBP1 T CELL OVARIAN CANCER
topic	IRE1 XBP1 T CELL OVARIAN CANCER
purl_subject.fl_str_mv	https://purl.org/becyt/ford/1.6 https://purl.org/becyt/ford/1 https://purl.org/becyt/ford/3.1 https://purl.org/becyt/ford/3 https://purl.org/becyt/ford/3.1 https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv	Tumours evade immune control by creating hostile microenvironments that perturb T cell metabolism and effector function 1?4 . However, it remains unclear how intra-tumoral T cells integrate and interpret metabolic stress signals. Here we report that ovarian cancer?an aggressive malignancy that is refractory to standard treatments and current immunotherapies 5?8 ?induces endoplasmic reticulum stress and activates the IRE1α?XBP1 arm of the unfolded protein response 9,10 in T cells to control their mitochondrial respiration and anti-tumour function. In T cells isolated from specimens collected from patients with ovarian cancer, upregulation of XBP1 was associated with decreased infiltration of T cells into tumours and with reduced IFNG mRNA expression. Malignant ascites fluid obtained from patients with ovarian cancer inhibited glucose uptake and caused N-linked protein glycosylation defects in T cells, which triggered IRE1α?XBP1 activation that suppressed mitochondrial activity and IFNγ production. Mechanistically, induction of XBP1 regulated the abundance of glutamine carriers and thus limited the influx of glutamine that is necessary to sustain mitochondrial respiration in T cells under glucose-deprived conditions. Restoring N-linked protein glycosylation, abrogating IRE1α?XBP1 activation or enforcing expression of glutamine transporters enhanced mitochondrial respiration in human T cells exposed to ovarian cancer ascites. XBP1-deficient T cells in the metastatic ovarian cancer milieu exhibited global transcriptional reprogramming and improved effector capacity. Accordingly, mice that bear ovarian cancer and lack XBP1 selectively in T cells demonstrate superior anti-tumour immunity, delayed malignant progression and increased overall survival. Controlling endoplasmic reticulum stress or targeting IRE1α?XBP1 signalling may help to restore the metabolic fitness and anti-tumour capacity of T cells in cancer hosts. Fil: Song, Minkyung. Weill Cornell Medicine; Estados Unidos Fil: Sandoval, Tito A.. Weill Cornell Medicine; Estados Unidos Fil: Chae, Chang-Suk. Weill Cornell Medicine; Estados Unidos Fil: Chopra, Sahil. Weill Cornell Medicine; Estados Unidos Fil: Tan, Chen. Weill Cornell Medicine; Estados Unidos Fil: Rutkowski, Melanie R.. University of Virginia; Estados Unidos Fil: Raundhal, Mahesh. Dana Farber Cancer Institute; Estados Unidos. Harvard Medical School; Estados Unidos Fil: Chaurio, Ricardo A.. H. Lee Moffitt Cancer Center & Research Institute; Estados Unidos Fil: Payne, Kyle K.. H. Lee Moffitt Cancer Center & Research Institute; Estados Unidos Fil: Konrad, Csaba. Weill Cornell Medicine; Estados Unidos Fil: Bettigole, Sarah E.. Quentis Therapeutics Inc.; Estados Unidos Fil: Shin, Hee Rae. Quentis Therapeutics Inc.; Estados Unidos Fil: Crowley, Michael J. P.. Weill Cornell Graduate School of Medical Sciences; Estados Unidos Fil: Cerliani, Juan Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina Fil: Kossenkov, Andrew V.. The Wistar Institute; Estados Unidos Fil: Motorykin, Ievgen. Weill Cornell Medicine,; Estados Unidos Fil: Zhang, Sheng. Weill Cornell Medicine,; Estados Unidos Fil: Manfredi, Giovanni. Weill Cornell Medicine,; Estados Unidos Fil: Zamarin, Dmitriy. Memorial Sloan Kettering Cancer Center; Estados Unidos Fil: Holcomb, Kevin. Weill Cornell Medicine,; Estados Unidos Fil: Rodriguez, Paulo C.. H. Lee Moffitt Cancer Center & Research Institute; Estados Unidos Fil: Rabinovich, Gabriel Adrián. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica; Argentina Fil: Conejo Garcia, Jose R.. H. Lee Moffitt Cancer Center & Research Institute; Estados Unidos Fil: Glimcher, Laurie H.. Dana Farber Cancer Institute; Estados Unidos. Harvard Medical School; Estados Unidos Fil: Cubillos-Ruiz, Juan R.. Weill Graduate School Of Medical Sciences; Estados Unidos. Weill Graduate School Of Medical Sciences; Estados Unidos
description	Tumours evade immune control by creating hostile microenvironments that perturb T cell metabolism and effector function 1?4 . However, it remains unclear how intra-tumoral T cells integrate and interpret metabolic stress signals. Here we report that ovarian cancer?an aggressive malignancy that is refractory to standard treatments and current immunotherapies 5?8 ?induces endoplasmic reticulum stress and activates the IRE1α?XBP1 arm of the unfolded protein response 9,10 in T cells to control their mitochondrial respiration and anti-tumour function. In T cells isolated from specimens collected from patients with ovarian cancer, upregulation of XBP1 was associated with decreased infiltration of T cells into tumours and with reduced IFNG mRNA expression. Malignant ascites fluid obtained from patients with ovarian cancer inhibited glucose uptake and caused N-linked protein glycosylation defects in T cells, which triggered IRE1α?XBP1 activation that suppressed mitochondrial activity and IFNγ production. Mechanistically, induction of XBP1 regulated the abundance of glutamine carriers and thus limited the influx of glutamine that is necessary to sustain mitochondrial respiration in T cells under glucose-deprived conditions. Restoring N-linked protein glycosylation, abrogating IRE1α?XBP1 activation or enforcing expression of glutamine transporters enhanced mitochondrial respiration in human T cells exposed to ovarian cancer ascites. XBP1-deficient T cells in the metastatic ovarian cancer milieu exhibited global transcriptional reprogramming and improved effector capacity. Accordingly, mice that bear ovarian cancer and lack XBP1 selectively in T cells demonstrate superior anti-tumour immunity, delayed malignant progression and increased overall survival. Controlling endoplasmic reticulum stress or targeting IRE1α?XBP1 signalling may help to restore the metabolic fitness and anti-tumour capacity of T cells in cancer hosts.
publishDate	2018
dc.date.none.fl_str_mv	2018-10
dc.type.none.fl_str_mv	info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion http://purl.org/coar/resource_type/c_6501 info:ar-repo/semantics/articulo
format	article
status_str	publishedVersion
dc.identifier.none.fl_str_mv	http://hdl.handle.net/11336/87374 Song, Minkyung; Sandoval, Tito A.; Chae, Chang-Suk; Chopra, Sahil; Tan, Chen; et al.; IRE1α–XBP1 controls T cell function in ovarian cancer by regulating mitochondrial activity; Nature Publishing Group; Nature; 562; 7727; 10-2018; 423-428 0028-0836 CONICET Digital CONICET
url	http://hdl.handle.net/11336/87374
identifier_str_mv	Song, Minkyung; Sandoval, Tito A.; Chae, Chang-Suk; Chopra, Sahil; Tan, Chen; et al.; IRE1α–XBP1 controls T cell function in ovarian cancer by regulating mitochondrial activity; Nature Publishing Group; Nature; 562; 7727; 10-2018; 423-428 0028-0836 CONICET Digital CONICET
dc.language.none.fl_str_mv	eng
language	eng
dc.relation.none.fl_str_mv	info:eu-repo/semantics/altIdentifier/doi/10.1038/s41586-018-0597-x info:eu-repo/semantics/altIdentifier/url/https://www.nature.com/articles/s41586-018-0597-x info:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/30305738/ info:eu-repo/semantics/altIdentifier/pmid/30305738
dc.rights.none.fl_str_mv	info:eu-repo/semantics/openAccess https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
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rights_invalid_str_mv	https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv	application/pdf application/pdf
dc.publisher.none.fl_str_mv	Nature Publishing Group
publisher.none.fl_str_mv	Nature Publishing Group
dc.source.none.fl_str_mv	reponame:CONICET Digital (CONICET) instname:Consejo Nacional de Investigaciones Científicas y Técnicas
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repository.mail.fl_str_mv	dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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IRE1α–XBP1 controls T cell function in ovarian cancer by regulating mitochondrial activity

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