Role played by the programmed death-1-programmed death ligand pathway during innate immunity against Mycobacterium tuberculosis
Tuberculous pleurisy allows the study of specific cells at the site of Mycobacterium tuberculosis infection. Among pleural lymphocytes, natural killer (NK) cells are a major source of interferon γ (IFN-γ), and their functions are regulated by activating and inhibitory receptors. Programmed death-1 (...
| Autores: | , , , , , , |
|---|---|
| Tipo de recurso: | artículo |
| Estado: | Versión publicada |
| Fecha de publicación: | 2010 |
| País: | Argentina |
| Institución: | Consejo Nacional de Investigaciones Científicas y Técnicas |
| Repositorio: | CONICET Digital (CONICET) |
| Idioma: | inglés |
| OAI Identifier: | oai:ri.conicet.gov.ar:11336/66505 |
| Acceso en línea: | http://hdl.handle.net/11336/66505 |
| Access Level: | acceso abierto |
| Palabra clave: | Tuberculosis Innate Immunity Costimulation Nk Cells https://purl.org/becyt/ford/1.6 https://purl.org/becyt/ford/1 |
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| dc.title.none.fl_str_mv |
Role played by the programmed death-1-programmed death ligand pathway during innate immunity against Mycobacterium tuberculosis |
| title |
Role played by the programmed death-1-programmed death ligand pathway during innate immunity against Mycobacterium tuberculosis |
| spellingShingle |
Role played by the programmed death-1-programmed death ligand pathway during innate immunity against Mycobacterium tuberculosis Alvarez, Ivana Belén Tuberculosis Innate Immunity Costimulation Nk Cells https://purl.org/becyt/ford/1.6 https://purl.org/becyt/ford/1 |
| title_short |
Role played by the programmed death-1-programmed death ligand pathway during innate immunity against Mycobacterium tuberculosis |
| title_full |
Role played by the programmed death-1-programmed death ligand pathway during innate immunity against Mycobacterium tuberculosis |
| title_fullStr |
Role played by the programmed death-1-programmed death ligand pathway during innate immunity against Mycobacterium tuberculosis |
| title_full_unstemmed |
Role played by the programmed death-1-programmed death ligand pathway during innate immunity against Mycobacterium tuberculosis |
| title_sort |
Role played by the programmed death-1-programmed death ligand pathway during innate immunity against Mycobacterium tuberculosis |
| dc.creator.none.fl_str_mv |
Alvarez, Ivana Belén Pasquinelli, Virginia Jurado, Javier Oscar Abbate, Pablo Eduardo Musella, Rosa María de la Barrera, Silvia Susana García, Verónica Edith |
| author |
Alvarez, Ivana Belén |
| author_facet |
Alvarez, Ivana Belén Pasquinelli, Virginia Jurado, Javier Oscar Abbate, Pablo Eduardo Musella, Rosa María de la Barrera, Silvia Susana García, Verónica Edith |
| author_role |
author |
| author2 |
Pasquinelli, Virginia Jurado, Javier Oscar Abbate, Pablo Eduardo Musella, Rosa María de la Barrera, Silvia Susana García, Verónica Edith |
| author2_role |
author author author author author author |
| dc.subject.none.fl_str_mv |
Tuberculosis Innate Immunity Costimulation Nk Cells https://purl.org/becyt/ford/1.6 https://purl.org/becyt/ford/1 |
| topic |
Tuberculosis Innate Immunity Costimulation Nk Cells https://purl.org/becyt/ford/1.6 https://purl.org/becyt/ford/1 |
| description |
Tuberculous pleurisy allows the study of specific cells at the site of Mycobacterium tuberculosis infection. Among pleural lymphocytes, natural killer (NK) cells are a major source of interferon γ (IFN-γ), and their functions are regulated by activating and inhibitory receptors. Programmed death-1 (PD-1), programmed death ligand 1 (PD-L1), and programmed death ligand 2 (PD-L2) are recognized inhibitory receptors in adaptive immunity, but their role during innate immunity remains poorly understood. We investigated the PD-1:PDL1/ PD-L2 pathway on NK cell effector functions in peripheral blood and pleural fluid from patients with tuberculosis. M. tuberculosis stimulation significantly up-regulated PD-1, PD-L1, and PD-L2 levels on NK cells. Interestingly, a direct correlation between PD-1 and IFN-γ expression on NK cells was observed. Moreover, blockade of the PD-1 pathway markedly augmented lytic degranulation and IFN-γ production of NK cells against M. tuberculosis. Furthermore, PD-1+ NK cells displayed a diminished IFN-γ mean fluorescence intensity, denoting the relevance of PD-1 on IFN-γ regulation. Together, we described a novel inhibitory role played by PD-1:PD-L interactions in innate immunity in tuberculosis. © 2010 by the Infectious Diseases Society of America. |
| publishDate |
2010 |
| dc.date.none.fl_str_mv |
2010-08 |
| 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/11336/66505 Alvarez, Ivana Belén; Pasquinelli, Virginia; Jurado, Javier Oscar; Abbate, Pablo Eduardo; Musella, Rosa María; et al.; Role played by the programmed death-1-programmed death ligand pathway during innate immunity against Mycobacterium tuberculosis; University of Chicago Press; Journal Of Infectious Diseases; 202; 4; 8-2010; 524-532 0022-1899 CONICET Digital CONICET |
| url |
http://hdl.handle.net/11336/66505 |
| identifier_str_mv |
Alvarez, Ivana Belén; Pasquinelli, Virginia; Jurado, Javier Oscar; Abbate, Pablo Eduardo; Musella, Rosa María; et al.; Role played by the programmed death-1-programmed death ligand pathway during innate immunity against Mycobacterium tuberculosis; University of Chicago Press; Journal Of Infectious Diseases; 202; 4; 8-2010; 524-532 0022-1899 CONICET Digital CONICET |
| dc.language.none.fl_str_mv |
eng |
| language |
eng |
| dc.relation.none.fl_str_mv |
info:eu-repo/semantics/altIdentifier/doi/10.1086/654932 info:eu-repo/semantics/altIdentifier/url/https://academic.oup.com/jid/article/202/4/524/2192187 |
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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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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 |
University of Chicago Press |
| publisher.none.fl_str_mv |
University of Chicago Press |
| dc.source.none.fl_str_mv |
reponame:CONICET Digital (CONICET) instname:Consejo Nacional de Investigaciones Científicas y Técnicas |
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Consejo Nacional de Investigaciones Científicas y Técnicas |
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CONICET Digital (CONICET) |
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CONICET Digital (CONICET) |
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CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas |
| repository.mail.fl_str_mv |
dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar |
| _version_ |
1799196072995717120 |
| spelling |
Role played by the programmed death-1-programmed death ligand pathway during innate immunity against Mycobacterium tuberculosisAlvarez, Ivana BelénPasquinelli, VirginiaJurado, Javier OscarAbbate, Pablo EduardoMusella, Rosa Maríade la Barrera, Silvia SusanaGarcía, Verónica EdithTuberculosisInnate ImmunityCostimulationNk Cellshttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Tuberculous pleurisy allows the study of specific cells at the site of Mycobacterium tuberculosis infection. Among pleural lymphocytes, natural killer (NK) cells are a major source of interferon γ (IFN-γ), and their functions are regulated by activating and inhibitory receptors. Programmed death-1 (PD-1), programmed death ligand 1 (PD-L1), and programmed death ligand 2 (PD-L2) are recognized inhibitory receptors in adaptive immunity, but their role during innate immunity remains poorly understood. We investigated the PD-1:PDL1/ PD-L2 pathway on NK cell effector functions in peripheral blood and pleural fluid from patients with tuberculosis. M. tuberculosis stimulation significantly up-regulated PD-1, PD-L1, and PD-L2 levels on NK cells. Interestingly, a direct correlation between PD-1 and IFN-γ expression on NK cells was observed. Moreover, blockade of the PD-1 pathway markedly augmented lytic degranulation and IFN-γ production of NK cells against M. tuberculosis. Furthermore, PD-1+ NK cells displayed a diminished IFN-γ mean fluorescence intensity, denoting the relevance of PD-1 on IFN-γ regulation. Together, we described a novel inhibitory role played by PD-1:PD-L interactions in innate immunity in tuberculosis. © 2010 by the Infectious Diseases Society of America.Fil: Alvarez, Ivana Belén. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica; ArgentinaFil: Pasquinelli, Virginia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica; ArgentinaFil: Jurado, Javier Oscar. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica; ArgentinaFil: Abbate, Pablo Eduardo. Gobierno de la Ciudad de Buenos Aires. Hospital de Infecciosas "Dr. Francisco Javier Muñiz"; ArgentinaFil: Musella, Rosa María. Gobierno de la Ciudad de Buenos Aires. Hospital de Infecciosas "Dr. Francisco Javier Muñiz"; ArgentinaFil: de la Barrera, Silvia Susana. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Academia Nacional de Medicina de Buenos Aires. Instituto de Investigaciones Hematológicas "Mariano R. Castex". Departamento de Inmunología y Medicina Experimental; ArgentinaFil: García, Verónica Edith. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica; ArgentinaUniversity of Chicago Press2010-08info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/66505Alvarez, Ivana Belén; Pasquinelli, Virginia; Jurado, Javier Oscar; Abbate, Pablo Eduardo; Musella, Rosa María; et al.; Role played by the programmed death-1-programmed death ligand pathway during innate immunity against Mycobacterium tuberculosis; University of Chicago Press; Journal Of Infectious Diseases; 202; 4; 8-2010; 524-5320022-1899CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1086/654932info:eu-repo/semantics/altIdentifier/url/https://academic.oup.com/jid/article/202/4/524/2192187info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2024-05-08T14:13:43Zoai:ri.conicet.gov.ar:11336/66505instacron: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:34982024-05-08 14:13:43.747CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
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15.812429 |