The C-Type Lectin Receptor DC-SIGN Has an Anti-Inflammatory Role in Human M(IL-4) Macrophages in Response to Mycobacterium tuberculosis.
- Autores
- Lugo Villarino, Geanncarlo; Troegeler, Anthony; Balboa, Luciana; Lastrucci, Claire; Duval, Carine; Mercier, Ingrid; Bénard, Alan; Capilla, Florence; Al Saati, Talal; Poincloux, Renaud; Kondova, Ivanela; Verreck, Frank A. W.; Cougoule, Céline; Maridonneau Parini, Isabelle; Sasiain, Maria del Carmen; Neyrolles, Olivier
- Año de publicación
- 2018
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- DC-SIGN (CD209/CLEC4L) is a C-type lectin receptor (CLR) that serves as a reliable cell-surface marker of interleukin 4 (IL-4)-activated human macrophages [M(IL-4)], which historically represent the most studied subset within the M2 spectrum of macrophage activation.Although DC-SIGN plays important roles in Mycobacterium tuberculosis (Mtb) interactions with dendritic cells, its contribution to the Mtb?macrophage interaction remains poorly understood. Since high levels of IL-4 are correlated with tuberculosis (TB) susceptibility andprogression, we investigated the role of DC-SIGN in M(IL-4) macrophages in the TB context. First, we demonstrate that DC-SIGN expression is present both in CD68+ macrophages found in tuberculous pulmonary lesions of non-human primates, and in the CD14+ cell population isolated from pleural effusions obtained from TB patients (TB-PE). Likewise, we showthat DC-SIGN expression is accentuated in M(IL-4) macrophages derived from peripheral blood CD14+ monocytes isolated from TB patients, or in macrophages stimulated with acellularTB-PE, arguing for the pertinence of DC-SIGN-expressing macrophages in TB. Second, using a siRNA-mediated gene silencing approach, we performed a transcriptomic analysis of DC-SIGN-depleted M(IL-4) macrophages and revealed the upregulation of pro-inflammatory signals in response to challenge with Mtb, as compared to control cells. This pro-inflammatorygene signature was confirmed by RT-qPCR, cytokine/chemokine-based protein array, and ELISA analyses. We also found that inactivation of DC-SIGN renders M(IL-4) macrophages less permissive to Mtb intracellular growth compared to control cells, despite the equal level of bacteria uptake. Last, at the molecular level, we show that DC-SIGN interferes negatively with the pro-inflammatory response and control of Mtb intracellular growth mediated by another CLR, Dectin-1 (CLEC7A). Collectively, this study highlights a dual role for DC-SIGN as, on the one hand, being a host factor granting advantage for Mtb to parasitize macrophages and, onthe other hand, representing a molecular switch to turn off the pro-inflammatory response in these cells to prevent potential immunopathology associated to TB.
Fil: Lugo Villarino, Geanncarlo. Centre National de la Recherche Scientifique; Francia
Fil: Troegeler, Anthony. 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: Lastrucci, Claire. Centre National de la Recherche Scientifique; Francia
Fil: Duval, Carine. Centre National de la Recherche Scientifique; Francia
Fil: Mercier, Ingrid. Centre National de la Recherche Scientifique; Francia
Fil: Bénard, Alan. Centre National de la Recherche Scientifique; Francia
Fil: Capilla, Florence. Inserm. Inmmunology- Immunopathology Immunotherapy; Francia
Fil: Al Saati, Talal. Inserm; Francia
Fil: Poincloux, Renaud. Centre National de la Recherche Scientifique; Francia
Fil: Kondova, Ivanela. No especifíca;
Fil: Verreck, Frank A. W.. No especifíca;
Fil: Cougoule, Céline. Centre National de la Recherche Scientifique; Francia
Fil: Maridonneau Parini, Isabelle. Centre National de la Recherche Scientifique; Francia
Fil: Sasiain, Maria 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 - Materia
-
MACROPHAGES
Mycobacteriun tuberculosis
DC-SIGN
C-TYPE LECTIN RECEPTORS - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
- Repositorio
.jpg)
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/239098
Ver los metadatos del registro completo
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The C-Type Lectin Receptor DC-SIGN Has an Anti-Inflammatory Role in Human M(IL-4) Macrophages in Response to Mycobacterium tuberculosis.Lugo Villarino, GeanncarloTroegeler, AnthonyBalboa, LucianaLastrucci, ClaireDuval, CarineMercier, IngridBénard, AlanCapilla, FlorenceAl Saati, TalalPoincloux, RenaudKondova, IvanelaVerreck, Frank A. W.Cougoule, CélineMaridonneau Parini, IsabelleSasiain, Maria del CarmenNeyrolles, OlivierMACROPHAGESMycobacteriun tuberculosisDC-SIGNC-TYPE LECTIN RECEPTORShttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3DC-SIGN (CD209/CLEC4L) is a C-type lectin receptor (CLR) that serves as a reliable cell-surface marker of interleukin 4 (IL-4)-activated human macrophages [M(IL-4)], which historically represent the most studied subset within the M2 spectrum of macrophage activation.Although DC-SIGN plays important roles in Mycobacterium tuberculosis (Mtb) interactions with dendritic cells, its contribution to the Mtb?macrophage interaction remains poorly understood. Since high levels of IL-4 are correlated with tuberculosis (TB) susceptibility andprogression, we investigated the role of DC-SIGN in M(IL-4) macrophages in the TB context. First, we demonstrate that DC-SIGN expression is present both in CD68+ macrophages found in tuberculous pulmonary lesions of non-human primates, and in the CD14+ cell population isolated from pleural effusions obtained from TB patients (TB-PE). Likewise, we showthat DC-SIGN expression is accentuated in M(IL-4) macrophages derived from peripheral blood CD14+ monocytes isolated from TB patients, or in macrophages stimulated with acellularTB-PE, arguing for the pertinence of DC-SIGN-expressing macrophages in TB. Second, using a siRNA-mediated gene silencing approach, we performed a transcriptomic analysis of DC-SIGN-depleted M(IL-4) macrophages and revealed the upregulation of pro-inflammatory signals in response to challenge with Mtb, as compared to control cells. This pro-inflammatorygene signature was confirmed by RT-qPCR, cytokine/chemokine-based protein array, and ELISA analyses. We also found that inactivation of DC-SIGN renders M(IL-4) macrophages less permissive to Mtb intracellular growth compared to control cells, despite the equal level of bacteria uptake. Last, at the molecular level, we show that DC-SIGN interferes negatively with the pro-inflammatory response and control of Mtb intracellular growth mediated by another CLR, Dectin-1 (CLEC7A). Collectively, this study highlights a dual role for DC-SIGN as, on the one hand, being a host factor granting advantage for Mtb to parasitize macrophages and, onthe other hand, representing a molecular switch to turn off the pro-inflammatory response in these cells to prevent potential immunopathology associated to TB.Fil: Lugo Villarino, Geanncarlo. Centre National de la Recherche Scientifique; FranciaFil: Troegeler, Anthony. 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: Lastrucci, Claire. Centre National de la Recherche Scientifique; FranciaFil: Duval, Carine. Centre National de la Recherche Scientifique; FranciaFil: Mercier, Ingrid. Centre National de la Recherche Scientifique; FranciaFil: Bénard, Alan. Centre National de la Recherche Scientifique; FranciaFil: Capilla, Florence. Inserm. Inmmunology- Immunopathology Immunotherapy; FranciaFil: Al Saati, Talal. Inserm; FranciaFil: Poincloux, Renaud. Centre National de la Recherche Scientifique; FranciaFil: Kondova, Ivanela. No especifíca;Fil: Verreck, Frank A. W.. No especifíca;Fil: Cougoule, Céline. Centre National de la Recherche Scientifique; FranciaFil: Maridonneau Parini, Isabelle. Centre National de la Recherche Scientifique; FranciaFil: Sasiain, Maria 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; FranciaFrontiers Media2018-06info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/239098Lugo Villarino, Geanncarlo; Troegeler, Anthony; Balboa, Luciana; Lastrucci, Claire; Duval, Carine; et al.; The C-Type Lectin Receptor DC-SIGN Has an Anti-Inflammatory Role in Human M(IL-4) Macrophages in Response to Mycobacterium tuberculosis.; Frontiers Media; Frontiers in Immunology; 9; 6-2018; 1-151664-3224CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.3389/fimmu.2018.01123info:eu-repo/semantics/altIdentifier/url/https://www.frontiersin.org/articles/10.3389/fimmu.2018.01123/fullinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T09:59:26Zoai:ri.conicet.gov.ar:11336/239098instacron: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:34982025-09-29 09:59:27.203CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
| dc.title.none.fl_str_mv |
The C-Type Lectin Receptor DC-SIGN Has an Anti-Inflammatory Role in Human M(IL-4) Macrophages in Response to Mycobacterium tuberculosis. |
| title |
The C-Type Lectin Receptor DC-SIGN Has an Anti-Inflammatory Role in Human M(IL-4) Macrophages in Response to Mycobacterium tuberculosis. |
| spellingShingle |
The C-Type Lectin Receptor DC-SIGN Has an Anti-Inflammatory Role in Human M(IL-4) Macrophages in Response to Mycobacterium tuberculosis. Lugo Villarino, Geanncarlo MACROPHAGES Mycobacteriun tuberculosis DC-SIGN C-TYPE LECTIN RECEPTORS |
| title_short |
The C-Type Lectin Receptor DC-SIGN Has an Anti-Inflammatory Role in Human M(IL-4) Macrophages in Response to Mycobacterium tuberculosis. |
| title_full |
The C-Type Lectin Receptor DC-SIGN Has an Anti-Inflammatory Role in Human M(IL-4) Macrophages in Response to Mycobacterium tuberculosis. |
| title_fullStr |
The C-Type Lectin Receptor DC-SIGN Has an Anti-Inflammatory Role in Human M(IL-4) Macrophages in Response to Mycobacterium tuberculosis. |
| title_full_unstemmed |
The C-Type Lectin Receptor DC-SIGN Has an Anti-Inflammatory Role in Human M(IL-4) Macrophages in Response to Mycobacterium tuberculosis. |
| title_sort |
The C-Type Lectin Receptor DC-SIGN Has an Anti-Inflammatory Role in Human M(IL-4) Macrophages in Response to Mycobacterium tuberculosis. |
| dc.creator.none.fl_str_mv |
Lugo Villarino, Geanncarlo Troegeler, Anthony Balboa, Luciana Lastrucci, Claire Duval, Carine Mercier, Ingrid Bénard, Alan Capilla, Florence Al Saati, Talal Poincloux, Renaud Kondova, Ivanela Verreck, Frank A. W. Cougoule, Céline Maridonneau Parini, Isabelle Sasiain, Maria del Carmen Neyrolles, Olivier |
| author |
Lugo Villarino, Geanncarlo |
| author_facet |
Lugo Villarino, Geanncarlo Troegeler, Anthony Balboa, Luciana Lastrucci, Claire Duval, Carine Mercier, Ingrid Bénard, Alan Capilla, Florence Al Saati, Talal Poincloux, Renaud Kondova, Ivanela Verreck, Frank A. W. Cougoule, Céline Maridonneau Parini, Isabelle Sasiain, Maria del Carmen Neyrolles, Olivier |
| author_role |
author |
| author2 |
Troegeler, Anthony Balboa, Luciana Lastrucci, Claire Duval, Carine Mercier, Ingrid Bénard, Alan Capilla, Florence Al Saati, Talal Poincloux, Renaud Kondova, Ivanela Verreck, Frank A. W. Cougoule, Céline Maridonneau Parini, Isabelle Sasiain, Maria del Carmen Neyrolles, Olivier |
| author2_role |
author author author author author author author author author author author author author author author |
| dc.subject.none.fl_str_mv |
MACROPHAGES Mycobacteriun tuberculosis DC-SIGN C-TYPE LECTIN RECEPTORS |
| topic |
MACROPHAGES Mycobacteriun tuberculosis DC-SIGN C-TYPE LECTIN RECEPTORS |
| purl_subject.fl_str_mv |
https://purl.org/becyt/ford/3.1 https://purl.org/becyt/ford/3 |
| dc.description.none.fl_txt_mv |
DC-SIGN (CD209/CLEC4L) is a C-type lectin receptor (CLR) that serves as a reliable cell-surface marker of interleukin 4 (IL-4)-activated human macrophages [M(IL-4)], which historically represent the most studied subset within the M2 spectrum of macrophage activation.Although DC-SIGN plays important roles in Mycobacterium tuberculosis (Mtb) interactions with dendritic cells, its contribution to the Mtb?macrophage interaction remains poorly understood. Since high levels of IL-4 are correlated with tuberculosis (TB) susceptibility andprogression, we investigated the role of DC-SIGN in M(IL-4) macrophages in the TB context. First, we demonstrate that DC-SIGN expression is present both in CD68+ macrophages found in tuberculous pulmonary lesions of non-human primates, and in the CD14+ cell population isolated from pleural effusions obtained from TB patients (TB-PE). Likewise, we showthat DC-SIGN expression is accentuated in M(IL-4) macrophages derived from peripheral blood CD14+ monocytes isolated from TB patients, or in macrophages stimulated with acellularTB-PE, arguing for the pertinence of DC-SIGN-expressing macrophages in TB. Second, using a siRNA-mediated gene silencing approach, we performed a transcriptomic analysis of DC-SIGN-depleted M(IL-4) macrophages and revealed the upregulation of pro-inflammatory signals in response to challenge with Mtb, as compared to control cells. This pro-inflammatorygene signature was confirmed by RT-qPCR, cytokine/chemokine-based protein array, and ELISA analyses. We also found that inactivation of DC-SIGN renders M(IL-4) macrophages less permissive to Mtb intracellular growth compared to control cells, despite the equal level of bacteria uptake. Last, at the molecular level, we show that DC-SIGN interferes negatively with the pro-inflammatory response and control of Mtb intracellular growth mediated by another CLR, Dectin-1 (CLEC7A). Collectively, this study highlights a dual role for DC-SIGN as, on the one hand, being a host factor granting advantage for Mtb to parasitize macrophages and, onthe other hand, representing a molecular switch to turn off the pro-inflammatory response in these cells to prevent potential immunopathology associated to TB. Fil: Lugo Villarino, Geanncarlo. Centre National de la Recherche Scientifique; Francia Fil: Troegeler, Anthony. 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: Lastrucci, Claire. Centre National de la Recherche Scientifique; Francia Fil: Duval, Carine. Centre National de la Recherche Scientifique; Francia Fil: Mercier, Ingrid. Centre National de la Recherche Scientifique; Francia Fil: Bénard, Alan. Centre National de la Recherche Scientifique; Francia Fil: Capilla, Florence. Inserm. Inmmunology- Immunopathology Immunotherapy; Francia Fil: Al Saati, Talal. Inserm; Francia Fil: Poincloux, Renaud. Centre National de la Recherche Scientifique; Francia Fil: Kondova, Ivanela. No especifíca; Fil: Verreck, Frank A. W.. No especifíca; Fil: Cougoule, Céline. Centre National de la Recherche Scientifique; Francia Fil: Maridonneau Parini, Isabelle. Centre National de la Recherche Scientifique; Francia Fil: Sasiain, Maria 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 |
| description |
DC-SIGN (CD209/CLEC4L) is a C-type lectin receptor (CLR) that serves as a reliable cell-surface marker of interleukin 4 (IL-4)-activated human macrophages [M(IL-4)], which historically represent the most studied subset within the M2 spectrum of macrophage activation.Although DC-SIGN plays important roles in Mycobacterium tuberculosis (Mtb) interactions with dendritic cells, its contribution to the Mtb?macrophage interaction remains poorly understood. Since high levels of IL-4 are correlated with tuberculosis (TB) susceptibility andprogression, we investigated the role of DC-SIGN in M(IL-4) macrophages in the TB context. First, we demonstrate that DC-SIGN expression is present both in CD68+ macrophages found in tuberculous pulmonary lesions of non-human primates, and in the CD14+ cell population isolated from pleural effusions obtained from TB patients (TB-PE). Likewise, we showthat DC-SIGN expression is accentuated in M(IL-4) macrophages derived from peripheral blood CD14+ monocytes isolated from TB patients, or in macrophages stimulated with acellularTB-PE, arguing for the pertinence of DC-SIGN-expressing macrophages in TB. Second, using a siRNA-mediated gene silencing approach, we performed a transcriptomic analysis of DC-SIGN-depleted M(IL-4) macrophages and revealed the upregulation of pro-inflammatory signals in response to challenge with Mtb, as compared to control cells. This pro-inflammatorygene signature was confirmed by RT-qPCR, cytokine/chemokine-based protein array, and ELISA analyses. We also found that inactivation of DC-SIGN renders M(IL-4) macrophages less permissive to Mtb intracellular growth compared to control cells, despite the equal level of bacteria uptake. Last, at the molecular level, we show that DC-SIGN interferes negatively with the pro-inflammatory response and control of Mtb intracellular growth mediated by another CLR, Dectin-1 (CLEC7A). Collectively, this study highlights a dual role for DC-SIGN as, on the one hand, being a host factor granting advantage for Mtb to parasitize macrophages and, onthe other hand, representing a molecular switch to turn off the pro-inflammatory response in these cells to prevent potential immunopathology associated to TB. |
| publishDate |
2018 |
| dc.date.none.fl_str_mv |
2018-06 |
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info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion http://purl.org/coar/resource_type/c_6501 info:ar-repo/semantics/articulo |
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article |
| status_str |
publishedVersion |
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http://hdl.handle.net/11336/239098 Lugo Villarino, Geanncarlo; Troegeler, Anthony; Balboa, Luciana; Lastrucci, Claire; Duval, Carine; et al.; The C-Type Lectin Receptor DC-SIGN Has an Anti-Inflammatory Role in Human M(IL-4) Macrophages in Response to Mycobacterium tuberculosis.; Frontiers Media; Frontiers in Immunology; 9; 6-2018; 1-15 1664-3224 CONICET Digital CONICET |
| url |
http://hdl.handle.net/11336/239098 |
| identifier_str_mv |
Lugo Villarino, Geanncarlo; Troegeler, Anthony; Balboa, Luciana; Lastrucci, Claire; Duval, Carine; et al.; The C-Type Lectin Receptor DC-SIGN Has an Anti-Inflammatory Role in Human M(IL-4) Macrophages in Response to Mycobacterium tuberculosis.; Frontiers Media; Frontiers in Immunology; 9; 6-2018; 1-15 1664-3224 CONICET Digital CONICET |
| dc.language.none.fl_str_mv |
eng |
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eng |
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info:eu-repo/semantics/altIdentifier/doi/10.3389/fimmu.2018.01123 info:eu-repo/semantics/altIdentifier/url/https://www.frontiersin.org/articles/10.3389/fimmu.2018.01123/full |
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info:eu-repo/semantics/openAccess https://creativecommons.org/licenses/by-nc-sa/2.5/ar/ |
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openAccess |
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Frontiers Media |
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Frontiers Media |
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CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas |
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dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar |
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