The down-modulation of IFN-Y-induced MHC-I expression by Brucella abortus RNA in CALU-6, HMEC and A-549 cells shares features with monocytes/macrophages'
- Autores
- Serafino, Agustina; Bertinat, Yasmín Ayelén; Bueno, Jorgelina; Pittaluga, Jose; Birnberg Weiss, Federico; Milillo, María Ayelén; Barrionuevo, Paula
- Año de publicación
- 2023
- Idioma
- español castellano
- Tipo de recurso
- documento de conferencia
- Estado
- versión publicada
- Descripción
- Brucella abortus (Ba) is an intracellular pathogen capable of surviving inside macrophages. Since the disease is presented in multiple forms, many different cells are susceptible to be infected by Ba. We previously demonstrated that Ba RNA is a vita-PAMP involved in the immune evasion mediated by this pathogen. One of the mechanisms displayed by Ba is the down-modulation of MHC-I on monocytes/macrophages when Th1 response is being held, i.e., in the presence of IFN-γ. Moreover, MHC-I total expression is not altered, instead these proteins are retained within the Golgi Apparatus (GA). More recently, we demonstrated that Ba RNA diminishes the IFN-γ-induced MHC-I surface expression in other cells able to be infected with Ba. However, we do not know if this phenomenon is due to the retention of MHC-I within the GA by Ba RNA, as occurs in human macrophages, their preferential niche. To evaluate this, we stimulated the human bronchial epithelium cell line (Calu-6), the human alveolar epithelium cell line (A549) and the endothelial microvasculature cell line (HMEC) with 10 µg/ml of Ba RNA in the presence of IFN-γ. After 48 h, MHC-I expression and GA marker GM130 were detected by confocal microscopy. We observed that Ba RNA induces colocalization of MHC-I and GM130 in Calu-6 and HMEC cells. However, no colocalization was detected in A-549 cells. Then, we evaluated the effect of Ba RNA on the secretion of IL-8, IL-6 and MCP-1. For this, Calu-6, A549 and HMEC cells were stimulated with Ba RNA (1, 5 and 10 μg/ml) in the presence of IFN-γ for 48 h. Afterwards, supernatants were collected and the secretion of IL-8, IL-6 and MCP-1 was quantified by sandwich ELISA. We did not observe any changes in MCP-1 in Ba RNA-treated cells. Conversely to what we expected, Calu-6, HMEC and A-549-Ba RNA-treated cells had higher IL-8 and IL-6 levels compared to those from untreated cells (p<0.05). In addition, our previous results indicate that Ba RNA inhibits the IFN-γ-induced MHC-I surface expression on human monocytes/macrophages by a TLR8-dependent mechanism and through the Epidermal Growth Factor Receptor (EGFR) pathway. In order to extend this finding Calu-6, A-549 and HMEC cells were stimulated with 10 µg/ml of Ba RNA in the presence of IFN-γ for 48 h. TLR-8 expression was confirmed by flow cytometry in all cell lines. Next, cells were stimulated with 10 µg/ml of Ba RNA in the presence of an EGFR ligand-blocking antibody (Cetuximab). Neutralization of the EGFR partially reversed the inhibition of MHC-I surface expression mediated by Ba RNA in HMEC and A549 cells. Overall, these results show that the down-modulation of MHC-I expression by Ba RNA in different cells susceptible to be infected by Ba would allow the bacteria to persist successfully within the host, remaining unnoticed and evading CD8+ T cell surveillance.
Fil: Serafino, Agustina. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina
Fil: Bertinat, Yasmín Ayelén. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina
Fil: Bueno, Jorgelina. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina
Fil: Pittaluga, Jose. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina
Fil: Birnberg Weiss, Federico. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina
Fil: Milillo, María Ayelén. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Patagonia Norte; Argentina. Universidad Nacional de Río Negro. Sede Andina. Centro de Estudios en Ciencia, Tecnología, Cultura y Desarrollo; Argentina
Fil: Barrionuevo, Paula. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina
LXXI Reunión Anual de la Sociedad Argentina de Inmunología
San Luis
Argentina
Sociedad Argentina de Inmunología - Materia
-
RNA
BRUCELLA ABORTUS
MHC-I
CALU-6
HMEC
MACROPHAGES - 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:11336/237491
Ver los metadatos del registro completo
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The down-modulation of IFN-Y-induced MHC-I expression by Brucella abortus RNA in CALU-6, HMEC and A-549 cells shares features with monocytes/macrophages'Serafino, AgustinaBertinat, Yasmín AyelénBueno, JorgelinaPittaluga, JoseBirnberg Weiss, FedericoMilillo, María AyelénBarrionuevo, PaulaRNABRUCELLA ABORTUSMHC-ICALU-6HMECMACROPHAGEShttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Brucella abortus (Ba) is an intracellular pathogen capable of surviving inside macrophages. Since the disease is presented in multiple forms, many different cells are susceptible to be infected by Ba. We previously demonstrated that Ba RNA is a vita-PAMP involved in the immune evasion mediated by this pathogen. One of the mechanisms displayed by Ba is the down-modulation of MHC-I on monocytes/macrophages when Th1 response is being held, i.e., in the presence of IFN-γ. Moreover, MHC-I total expression is not altered, instead these proteins are retained within the Golgi Apparatus (GA). More recently, we demonstrated that Ba RNA diminishes the IFN-γ-induced MHC-I surface expression in other cells able to be infected with Ba. However, we do not know if this phenomenon is due to the retention of MHC-I within the GA by Ba RNA, as occurs in human macrophages, their preferential niche. To evaluate this, we stimulated the human bronchial epithelium cell line (Calu-6), the human alveolar epithelium cell line (A549) and the endothelial microvasculature cell line (HMEC) with 10 µg/ml of Ba RNA in the presence of IFN-γ. After 48 h, MHC-I expression and GA marker GM130 were detected by confocal microscopy. We observed that Ba RNA induces colocalization of MHC-I and GM130 in Calu-6 and HMEC cells. However, no colocalization was detected in A-549 cells. Then, we evaluated the effect of Ba RNA on the secretion of IL-8, IL-6 and MCP-1. For this, Calu-6, A549 and HMEC cells were stimulated with Ba RNA (1, 5 and 10 μg/ml) in the presence of IFN-γ for 48 h. Afterwards, supernatants were collected and the secretion of IL-8, IL-6 and MCP-1 was quantified by sandwich ELISA. We did not observe any changes in MCP-1 in Ba RNA-treated cells. Conversely to what we expected, Calu-6, HMEC and A-549-Ba RNA-treated cells had higher IL-8 and IL-6 levels compared to those from untreated cells (p<0.05). In addition, our previous results indicate that Ba RNA inhibits the IFN-γ-induced MHC-I surface expression on human monocytes/macrophages by a TLR8-dependent mechanism and through the Epidermal Growth Factor Receptor (EGFR) pathway. In order to extend this finding Calu-6, A-549 and HMEC cells were stimulated with 10 µg/ml of Ba RNA in the presence of IFN-γ for 48 h. TLR-8 expression was confirmed by flow cytometry in all cell lines. Next, cells were stimulated with 10 µg/ml of Ba RNA in the presence of an EGFR ligand-blocking antibody (Cetuximab). Neutralization of the EGFR partially reversed the inhibition of MHC-I surface expression mediated by Ba RNA in HMEC and A549 cells. Overall, these results show that the down-modulation of MHC-I expression by Ba RNA in different cells susceptible to be infected by Ba would allow the bacteria to persist successfully within the host, remaining unnoticed and evading CD8+ T cell surveillance.Fil: Serafino, Agustina. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Bertinat, Yasmín Ayelén. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Bueno, Jorgelina. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Pittaluga, Jose. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Birnberg Weiss, Federico. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Milillo, María Ayelén. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Patagonia Norte; Argentina. Universidad Nacional de Río Negro. Sede Andina. Centro de Estudios en Ciencia, Tecnología, Cultura y Desarrollo; ArgentinaFil: Barrionuevo, Paula. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaLXXI Reunión Anual de la Sociedad Argentina de InmunologíaSan LuisArgentinaSociedad Argentina de InmunologíaUniversidad Nacional de San Luis2023info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/conferenceObjectReuniónBookhttp://purl.org/coar/resource_type/c_5794info:ar-repo/semantics/documentoDeConferenciaapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/237491The down-modulation of IFN-Y-induced MHC-I expression by Brucella abortus RNA in CALU-6, HMEC and A-549 cells shares features with monocytes/macrophages'; LXXI Reunión Anual de la Sociedad Argentina de Inmunología; San Luis; Argentina; 2023; 77-77978-987-733-386-2CONICET DigitalCONICETspainfo:eu-repo/semantics/altIdentifier/url/https://inmunologia.org.ar/reunion-anual-2023/info:eu-repo/semantics/altIdentifier/url/https://inmunologia.org.ar/wp-content/uploads/2023/11/Libro-de-Resumenes-LXXI-Reunion-SAI-2023.pdfNacionalinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:58:32Zoai:ri.conicet.gov.ar:11336/237491instacron: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:34982025-09-03 09:58:32.669CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
| dc.title.none.fl_str_mv |
The down-modulation of IFN-Y-induced MHC-I expression by Brucella abortus RNA in CALU-6, HMEC and A-549 cells shares features with monocytes/macrophages' |
| title |
The down-modulation of IFN-Y-induced MHC-I expression by Brucella abortus RNA in CALU-6, HMEC and A-549 cells shares features with monocytes/macrophages' |
| spellingShingle |
The down-modulation of IFN-Y-induced MHC-I expression by Brucella abortus RNA in CALU-6, HMEC and A-549 cells shares features with monocytes/macrophages' Serafino, Agustina RNA BRUCELLA ABORTUS MHC-I CALU-6 HMEC MACROPHAGES |
| title_short |
The down-modulation of IFN-Y-induced MHC-I expression by Brucella abortus RNA in CALU-6, HMEC and A-549 cells shares features with monocytes/macrophages' |
| title_full |
The down-modulation of IFN-Y-induced MHC-I expression by Brucella abortus RNA in CALU-6, HMEC and A-549 cells shares features with monocytes/macrophages' |
| title_fullStr |
The down-modulation of IFN-Y-induced MHC-I expression by Brucella abortus RNA in CALU-6, HMEC and A-549 cells shares features with monocytes/macrophages' |
| title_full_unstemmed |
The down-modulation of IFN-Y-induced MHC-I expression by Brucella abortus RNA in CALU-6, HMEC and A-549 cells shares features with monocytes/macrophages' |
| title_sort |
The down-modulation of IFN-Y-induced MHC-I expression by Brucella abortus RNA in CALU-6, HMEC and A-549 cells shares features with monocytes/macrophages' |
| dc.creator.none.fl_str_mv |
Serafino, Agustina Bertinat, Yasmín Ayelén Bueno, Jorgelina Pittaluga, Jose Birnberg Weiss, Federico Milillo, María Ayelén Barrionuevo, Paula |
| author |
Serafino, Agustina |
| author_facet |
Serafino, Agustina Bertinat, Yasmín Ayelén Bueno, Jorgelina Pittaluga, Jose Birnberg Weiss, Federico Milillo, María Ayelén Barrionuevo, Paula |
| author_role |
author |
| author2 |
Bertinat, Yasmín Ayelén Bueno, Jorgelina Pittaluga, Jose Birnberg Weiss, Federico Milillo, María Ayelén Barrionuevo, Paula |
| author2_role |
author author author author author author |
| dc.subject.none.fl_str_mv |
RNA BRUCELLA ABORTUS MHC-I CALU-6 HMEC MACROPHAGES |
| topic |
RNA BRUCELLA ABORTUS MHC-I CALU-6 HMEC MACROPHAGES |
| purl_subject.fl_str_mv |
https://purl.org/becyt/ford/3.1 https://purl.org/becyt/ford/3 |
| dc.description.none.fl_txt_mv |
Brucella abortus (Ba) is an intracellular pathogen capable of surviving inside macrophages. Since the disease is presented in multiple forms, many different cells are susceptible to be infected by Ba. We previously demonstrated that Ba RNA is a vita-PAMP involved in the immune evasion mediated by this pathogen. One of the mechanisms displayed by Ba is the down-modulation of MHC-I on monocytes/macrophages when Th1 response is being held, i.e., in the presence of IFN-γ. Moreover, MHC-I total expression is not altered, instead these proteins are retained within the Golgi Apparatus (GA). More recently, we demonstrated that Ba RNA diminishes the IFN-γ-induced MHC-I surface expression in other cells able to be infected with Ba. However, we do not know if this phenomenon is due to the retention of MHC-I within the GA by Ba RNA, as occurs in human macrophages, their preferential niche. To evaluate this, we stimulated the human bronchial epithelium cell line (Calu-6), the human alveolar epithelium cell line (A549) and the endothelial microvasculature cell line (HMEC) with 10 µg/ml of Ba RNA in the presence of IFN-γ. After 48 h, MHC-I expression and GA marker GM130 were detected by confocal microscopy. We observed that Ba RNA induces colocalization of MHC-I and GM130 in Calu-6 and HMEC cells. However, no colocalization was detected in A-549 cells. Then, we evaluated the effect of Ba RNA on the secretion of IL-8, IL-6 and MCP-1. For this, Calu-6, A549 and HMEC cells were stimulated with Ba RNA (1, 5 and 10 μg/ml) in the presence of IFN-γ for 48 h. Afterwards, supernatants were collected and the secretion of IL-8, IL-6 and MCP-1 was quantified by sandwich ELISA. We did not observe any changes in MCP-1 in Ba RNA-treated cells. Conversely to what we expected, Calu-6, HMEC and A-549-Ba RNA-treated cells had higher IL-8 and IL-6 levels compared to those from untreated cells (p<0.05). In addition, our previous results indicate that Ba RNA inhibits the IFN-γ-induced MHC-I surface expression on human monocytes/macrophages by a TLR8-dependent mechanism and through the Epidermal Growth Factor Receptor (EGFR) pathway. In order to extend this finding Calu-6, A-549 and HMEC cells were stimulated with 10 µg/ml of Ba RNA in the presence of IFN-γ for 48 h. TLR-8 expression was confirmed by flow cytometry in all cell lines. Next, cells were stimulated with 10 µg/ml of Ba RNA in the presence of an EGFR ligand-blocking antibody (Cetuximab). Neutralization of the EGFR partially reversed the inhibition of MHC-I surface expression mediated by Ba RNA in HMEC and A549 cells. Overall, these results show that the down-modulation of MHC-I expression by Ba RNA in different cells susceptible to be infected by Ba would allow the bacteria to persist successfully within the host, remaining unnoticed and evading CD8+ T cell surveillance. Fil: Serafino, Agustina. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina Fil: Bertinat, Yasmín Ayelén. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina Fil: Bueno, Jorgelina. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina Fil: Pittaluga, Jose. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina Fil: Birnberg Weiss, Federico. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina Fil: Milillo, María Ayelén. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Patagonia Norte; Argentina. Universidad Nacional de Río Negro. Sede Andina. Centro de Estudios en Ciencia, Tecnología, Cultura y Desarrollo; Argentina Fil: Barrionuevo, Paula. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina LXXI Reunión Anual de la Sociedad Argentina de Inmunología San Luis Argentina Sociedad Argentina de Inmunología |
| description |
Brucella abortus (Ba) is an intracellular pathogen capable of surviving inside macrophages. Since the disease is presented in multiple forms, many different cells are susceptible to be infected by Ba. We previously demonstrated that Ba RNA is a vita-PAMP involved in the immune evasion mediated by this pathogen. One of the mechanisms displayed by Ba is the down-modulation of MHC-I on monocytes/macrophages when Th1 response is being held, i.e., in the presence of IFN-γ. Moreover, MHC-I total expression is not altered, instead these proteins are retained within the Golgi Apparatus (GA). More recently, we demonstrated that Ba RNA diminishes the IFN-γ-induced MHC-I surface expression in other cells able to be infected with Ba. However, we do not know if this phenomenon is due to the retention of MHC-I within the GA by Ba RNA, as occurs in human macrophages, their preferential niche. To evaluate this, we stimulated the human bronchial epithelium cell line (Calu-6), the human alveolar epithelium cell line (A549) and the endothelial microvasculature cell line (HMEC) with 10 µg/ml of Ba RNA in the presence of IFN-γ. After 48 h, MHC-I expression and GA marker GM130 were detected by confocal microscopy. We observed that Ba RNA induces colocalization of MHC-I and GM130 in Calu-6 and HMEC cells. However, no colocalization was detected in A-549 cells. Then, we evaluated the effect of Ba RNA on the secretion of IL-8, IL-6 and MCP-1. For this, Calu-6, A549 and HMEC cells were stimulated with Ba RNA (1, 5 and 10 μg/ml) in the presence of IFN-γ for 48 h. Afterwards, supernatants were collected and the secretion of IL-8, IL-6 and MCP-1 was quantified by sandwich ELISA. We did not observe any changes in MCP-1 in Ba RNA-treated cells. Conversely to what we expected, Calu-6, HMEC and A-549-Ba RNA-treated cells had higher IL-8 and IL-6 levels compared to those from untreated cells (p<0.05). In addition, our previous results indicate that Ba RNA inhibits the IFN-γ-induced MHC-I surface expression on human monocytes/macrophages by a TLR8-dependent mechanism and through the Epidermal Growth Factor Receptor (EGFR) pathway. In order to extend this finding Calu-6, A-549 and HMEC cells were stimulated with 10 µg/ml of Ba RNA in the presence of IFN-γ for 48 h. TLR-8 expression was confirmed by flow cytometry in all cell lines. Next, cells were stimulated with 10 µg/ml of Ba RNA in the presence of an EGFR ligand-blocking antibody (Cetuximab). Neutralization of the EGFR partially reversed the inhibition of MHC-I surface expression mediated by Ba RNA in HMEC and A549 cells. Overall, these results show that the down-modulation of MHC-I expression by Ba RNA in different cells susceptible to be infected by Ba would allow the bacteria to persist successfully within the host, remaining unnoticed and evading CD8+ T cell surveillance. |
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2023 |
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