Tuberculosis is associated with expansion of a motile, permissive and immunomodulatory CD16(+) monocyte population via the IL-10/STAT3 axis

Autores
Lastrucci, Claire; Bénard, Alan; Balboa, Luciana; Pingris, Karine; Souriant, Shanti; Poincloux, Renaud; Al Saati, Talal; Rasolofo, Voahangy; González Montaner, Pablo; Inwentarz, Sandra; Moraña, Eduardo José; Kondova, Ivanela; Verreck, Franck A. W.; Sasiain, María del Carmen; Neyrolles, Olivier; Maridonneau Parini, Isabel; Lugo Villarino, Geanncarlo; Cougoule, Celine
Año de publicación
2015
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
The human CD14+ monocyte compartment is composed by two subsets based on CD16 expression. We previously reported that this compartment is perturbed in tuberculosis (TB) patients, as reflected by the expansion of CD16+ monocytes along with disease severity. Whether this unbalance is beneficial or detrimental to host defense remains to be elucidated. Here in the context of active TB, we demonstrate that human monocytes are predisposed to differentiate towards an anti-inflammatory (M2-like) macrophage activation program characterized by theCD16+CD163+MerTK+pSTAT3+ phenotype and functional properties such as enhanced protease-dependent motility, pathogen permissivity and immunomodulation. This process is dependent on STAT3 activation, and loss-of-function experiments point towards a detrimental role in host defense against TB. Importantly, we provide a critical correlation between the abundance of the CD16+CD163+MerTK+pSTAT3+ cells and the progression of the disease either at the local level in a non-human primate tuberculous granuloma context, or at the systemic level through the detection of the soluble form of CD163 in human sera. Collectively, this study argues for the pathogenic role of the CD16+CD163+MerTK+pSTAT3+ monocyte-to-macrophage differentiation program and its potential as a target for TB therapy,and promotes the detection of circulating CD163 as a potential biomarker for disease progression and monitoringof treatment efficacy.
Fil: Lastrucci, Claire. Centre National de la Recherche Scientifique; Francia
Fil: Bénard, Alan. Centre National de la Recherche Scientifique; Francia
Fil: Balboa, Luciana. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina
Fil: Pingris, Karine. Centre National de la Recherche Scientifique; Francia
Fil: Souriant, Shanti. Centre National de la Recherche Scientifique; Francia
Fil: Poincloux, Renaud. Centre National de la Recherche Scientifique; Francia
Fil: Al Saati, Talal. Inserm; Francia
Fil: Rasolofo, Voahangy. Pasteur Institute in Antananarivo; Madagascar
Fil: González Montaner, Pablo. Gobierno de la Ciudad de Buenos Aires. Hospital de Infecciosas ; Argentina
Fil: Inwentarz, Sandra. Gobierno de la Ciudad de Buenos Aires. Hospital de Infecciosas ; Argentina
Fil: Moraña, Eduardo José. Gobierno de la Ciudad de Buenos Aires. Hospital de Infecciosas ; Argentina
Fil: Kondova, Ivanela. Biomedical Primate Research Centre; Países Bajos
Fil: Verreck, Franck A. W.. Biomedical Primate Research Centre; Países Bajos
Fil: Sasiain, María del Carmen. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina
Fil: Neyrolles, Olivier. Centre National de la Recherche Scientifique; Francia
Fil: Maridonneau Parini, Isabel. Centre National de la Recherche Scientifique; Francia
Fil: Lugo Villarino, Geanncarlo. Centre National de la Recherche Scientifique; Francia
Fil: Cougoule, Celine. Centre National de la Recherche Scientifique; Francia
Materia
Tuberculosis
Stat3
Monocyte
Macrophage Activation
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/42757

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spelling Tuberculosis is associated with expansion of a motile, permissive and immunomodulatory CD16(+) monocyte population via the IL-10/STAT3 axisLastrucci, ClaireBénard, AlanBalboa, LucianaPingris, KarineSouriant, ShantiPoincloux, RenaudAl Saati, TalalRasolofo, VoahangyGonzález Montaner, PabloInwentarz, SandraMoraña, Eduardo JoséKondova, IvanelaVerreck, Franck A. W.Sasiain, María del CarmenNeyrolles, OlivierMaridonneau Parini, IsabelLugo Villarino, GeanncarloCougoule, CelineTuberculosisStat3MonocyteMacrophage Activationhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3https://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3The human CD14+ monocyte compartment is composed by two subsets based on CD16 expression. We previously reported that this compartment is perturbed in tuberculosis (TB) patients, as reflected by the expansion of CD16+ monocytes along with disease severity. Whether this unbalance is beneficial or detrimental to host defense remains to be elucidated. Here in the context of active TB, we demonstrate that human monocytes are predisposed to differentiate towards an anti-inflammatory (M2-like) macrophage activation program characterized by theCD16+CD163+MerTK+pSTAT3+ phenotype and functional properties such as enhanced protease-dependent motility, pathogen permissivity and immunomodulation. This process is dependent on STAT3 activation, and loss-of-function experiments point towards a detrimental role in host defense against TB. Importantly, we provide a critical correlation between the abundance of the CD16+CD163+MerTK+pSTAT3+ cells and the progression of the disease either at the local level in a non-human primate tuberculous granuloma context, or at the systemic level through the detection of the soluble form of CD163 in human sera. Collectively, this study argues for the pathogenic role of the CD16+CD163+MerTK+pSTAT3+ monocyte-to-macrophage differentiation program and its potential as a target for TB therapy,and promotes the detection of circulating CD163 as a potential biomarker for disease progression and monitoringof treatment efficacy.Fil: Lastrucci, Claire. Centre National de la Recherche Scientifique; FranciaFil: Bénard, Alan. Centre National de la Recherche Scientifique; FranciaFil: Balboa, Luciana. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Pingris, Karine. Centre National de la Recherche Scientifique; FranciaFil: Souriant, Shanti. Centre National de la Recherche Scientifique; FranciaFil: Poincloux, Renaud. Centre National de la Recherche Scientifique; FranciaFil: Al Saati, Talal. Inserm; FranciaFil: Rasolofo, Voahangy. Pasteur Institute in Antananarivo; MadagascarFil: González Montaner, Pablo. Gobierno de la Ciudad de Buenos Aires. Hospital de Infecciosas ; ArgentinaFil: Inwentarz, Sandra. Gobierno de la Ciudad de Buenos Aires. Hospital de Infecciosas ; ArgentinaFil: Moraña, Eduardo José. Gobierno de la Ciudad de Buenos Aires. Hospital de Infecciosas ; ArgentinaFil: Kondova, Ivanela. Biomedical Primate Research Centre; Países BajosFil: Verreck, Franck A. W.. Biomedical Primate Research Centre; Países BajosFil: Sasiain, María del Carmen. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Neyrolles, Olivier. Centre National de la Recherche Scientifique; FranciaFil: Maridonneau Parini, Isabel. Centre National de la Recherche Scientifique; FranciaFil: Lugo Villarino, Geanncarlo. Centre National de la Recherche Scientifique; FranciaFil: Cougoule, Celine. Centre National de la Recherche Scientifique; FranciaInst Biochemistry & Cell Biology2015-10-20info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/42757Lastrucci, Claire; Bénard, Alan; Balboa, Luciana; Pingris, Karine; Souriant, Shanti; et al.; Tuberculosis is associated with expansion of a motile, permissive and immunomodulatory CD16(+) monocyte population via the IL-10/STAT3 axis; Inst Biochemistry & Cell Biology; Cell Research; 25; 20-10-2015; 1333-13511001-06021748-7838CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.nature.com/articles/cr2015123info:eu-repo/semantics/altIdentifier/doi/10.1038/cr.2015.123info:eu-repo/semantics/altIdentifier/pmid/26482950info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-15T15:04:57Zoai:ri.conicet.gov.ar:11336/42757instacron: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 15:04:57.428CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Tuberculosis is associated with expansion of a motile, permissive and immunomodulatory CD16(+) monocyte population via the IL-10/STAT3 axis
title Tuberculosis is associated with expansion of a motile, permissive and immunomodulatory CD16(+) monocyte population via the IL-10/STAT3 axis
spellingShingle Tuberculosis is associated with expansion of a motile, permissive and immunomodulatory CD16(+) monocyte population via the IL-10/STAT3 axis
Lastrucci, Claire
Tuberculosis
Stat3
Monocyte
Macrophage Activation
title_short Tuberculosis is associated with expansion of a motile, permissive and immunomodulatory CD16(+) monocyte population via the IL-10/STAT3 axis
title_full Tuberculosis is associated with expansion of a motile, permissive and immunomodulatory CD16(+) monocyte population via the IL-10/STAT3 axis
title_fullStr Tuberculosis is associated with expansion of a motile, permissive and immunomodulatory CD16(+) monocyte population via the IL-10/STAT3 axis
title_full_unstemmed Tuberculosis is associated with expansion of a motile, permissive and immunomodulatory CD16(+) monocyte population via the IL-10/STAT3 axis
title_sort Tuberculosis is associated with expansion of a motile, permissive and immunomodulatory CD16(+) monocyte population via the IL-10/STAT3 axis
dc.creator.none.fl_str_mv Lastrucci, Claire
Bénard, Alan
Balboa, Luciana
Pingris, Karine
Souriant, Shanti
Poincloux, Renaud
Al Saati, Talal
Rasolofo, Voahangy
González Montaner, Pablo
Inwentarz, Sandra
Moraña, Eduardo José
Kondova, Ivanela
Verreck, Franck A. W.
Sasiain, María del Carmen
Neyrolles, Olivier
Maridonneau Parini, Isabel
Lugo Villarino, Geanncarlo
Cougoule, Celine
author Lastrucci, Claire
author_facet Lastrucci, Claire
Bénard, Alan
Balboa, Luciana
Pingris, Karine
Souriant, Shanti
Poincloux, Renaud
Al Saati, Talal
Rasolofo, Voahangy
González Montaner, Pablo
Inwentarz, Sandra
Moraña, Eduardo José
Kondova, Ivanela
Verreck, Franck A. W.
Sasiain, María del Carmen
Neyrolles, Olivier
Maridonneau Parini, Isabel
Lugo Villarino, Geanncarlo
Cougoule, Celine
author_role author
author2 Bénard, Alan
Balboa, Luciana
Pingris, Karine
Souriant, Shanti
Poincloux, Renaud
Al Saati, Talal
Rasolofo, Voahangy
González Montaner, Pablo
Inwentarz, Sandra
Moraña, Eduardo José
Kondova, Ivanela
Verreck, Franck A. W.
Sasiain, María del Carmen
Neyrolles, Olivier
Maridonneau Parini, Isabel
Lugo Villarino, Geanncarlo
Cougoule, Celine
author2_role author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Tuberculosis
Stat3
Monocyte
Macrophage Activation
topic Tuberculosis
Stat3
Monocyte
Macrophage Activation
purl_subject.fl_str_mv 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 The human CD14+ monocyte compartment is composed by two subsets based on CD16 expression. We previously reported that this compartment is perturbed in tuberculosis (TB) patients, as reflected by the expansion of CD16+ monocytes along with disease severity. Whether this unbalance is beneficial or detrimental to host defense remains to be elucidated. Here in the context of active TB, we demonstrate that human monocytes are predisposed to differentiate towards an anti-inflammatory (M2-like) macrophage activation program characterized by theCD16+CD163+MerTK+pSTAT3+ phenotype and functional properties such as enhanced protease-dependent motility, pathogen permissivity and immunomodulation. This process is dependent on STAT3 activation, and loss-of-function experiments point towards a detrimental role in host defense against TB. Importantly, we provide a critical correlation between the abundance of the CD16+CD163+MerTK+pSTAT3+ cells and the progression of the disease either at the local level in a non-human primate tuberculous granuloma context, or at the systemic level through the detection of the soluble form of CD163 in human sera. Collectively, this study argues for the pathogenic role of the CD16+CD163+MerTK+pSTAT3+ monocyte-to-macrophage differentiation program and its potential as a target for TB therapy,and promotes the detection of circulating CD163 as a potential biomarker for disease progression and monitoringof treatment efficacy.
Fil: Lastrucci, Claire. Centre National de la Recherche Scientifique; Francia
Fil: Bénard, Alan. Centre National de la Recherche Scientifique; Francia
Fil: Balboa, Luciana. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina
Fil: Pingris, Karine. Centre National de la Recherche Scientifique; Francia
Fil: Souriant, Shanti. Centre National de la Recherche Scientifique; Francia
Fil: Poincloux, Renaud. Centre National de la Recherche Scientifique; Francia
Fil: Al Saati, Talal. Inserm; Francia
Fil: Rasolofo, Voahangy. Pasteur Institute in Antananarivo; Madagascar
Fil: González Montaner, Pablo. Gobierno de la Ciudad de Buenos Aires. Hospital de Infecciosas ; Argentina
Fil: Inwentarz, Sandra. Gobierno de la Ciudad de Buenos Aires. Hospital de Infecciosas ; Argentina
Fil: Moraña, Eduardo José. Gobierno de la Ciudad de Buenos Aires. Hospital de Infecciosas ; Argentina
Fil: Kondova, Ivanela. Biomedical Primate Research Centre; Países Bajos
Fil: Verreck, Franck A. W.. Biomedical Primate Research Centre; Países Bajos
Fil: Sasiain, María del Carmen. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina
Fil: Neyrolles, Olivier. Centre National de la Recherche Scientifique; Francia
Fil: Maridonneau Parini, Isabel. Centre National de la Recherche Scientifique; Francia
Fil: Lugo Villarino, Geanncarlo. Centre National de la Recherche Scientifique; Francia
Fil: Cougoule, Celine. Centre National de la Recherche Scientifique; Francia
description The human CD14+ monocyte compartment is composed by two subsets based on CD16 expression. We previously reported that this compartment is perturbed in tuberculosis (TB) patients, as reflected by the expansion of CD16+ monocytes along with disease severity. Whether this unbalance is beneficial or detrimental to host defense remains to be elucidated. Here in the context of active TB, we demonstrate that human monocytes are predisposed to differentiate towards an anti-inflammatory (M2-like) macrophage activation program characterized by theCD16+CD163+MerTK+pSTAT3+ phenotype and functional properties such as enhanced protease-dependent motility, pathogen permissivity and immunomodulation. This process is dependent on STAT3 activation, and loss-of-function experiments point towards a detrimental role in host defense against TB. Importantly, we provide a critical correlation between the abundance of the CD16+CD163+MerTK+pSTAT3+ cells and the progression of the disease either at the local level in a non-human primate tuberculous granuloma context, or at the systemic level through the detection of the soluble form of CD163 in human sera. Collectively, this study argues for the pathogenic role of the CD16+CD163+MerTK+pSTAT3+ monocyte-to-macrophage differentiation program and its potential as a target for TB therapy,and promotes the detection of circulating CD163 as a potential biomarker for disease progression and monitoringof treatment efficacy.
publishDate 2015
dc.date.none.fl_str_mv 2015-10-20
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/11336/42757
Lastrucci, Claire; Bénard, Alan; Balboa, Luciana; Pingris, Karine; Souriant, Shanti; et al.; Tuberculosis is associated with expansion of a motile, permissive and immunomodulatory CD16(+) monocyte population via the IL-10/STAT3 axis; Inst Biochemistry & Cell Biology; Cell Research; 25; 20-10-2015; 1333-1351
1001-0602
1748-7838
CONICET Digital
CONICET
url http://hdl.handle.net/11336/42757
identifier_str_mv Lastrucci, Claire; Bénard, Alan; Balboa, Luciana; Pingris, Karine; Souriant, Shanti; et al.; Tuberculosis is associated with expansion of a motile, permissive and immunomodulatory CD16(+) monocyte population via the IL-10/STAT3 axis; Inst Biochemistry & Cell Biology; Cell Research; 25; 20-10-2015; 1333-1351
1001-0602
1748-7838
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://www.nature.com/articles/cr2015123
info:eu-repo/semantics/altIdentifier/doi/10.1038/cr.2015.123
info:eu-repo/semantics/altIdentifier/pmid/26482950
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
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 Inst Biochemistry & Cell Biology
publisher.none.fl_str_mv Inst Biochemistry & Cell Biology
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
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instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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