Inducible Costimulator: A Modulator of IFN-γ Production in Human Tuberculosis

Autores
Quiroga, María Florencia; Pasquinelli, Virginia; Martínez, Gustavo J.; Jurado, Javier Oscar; Zorrilla, Liliana Castro; Musella, Rosa María; Abbate, Eduardo José; Sieling, Peter A.; García, Verónica Edith
Año de publicación
2006
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Effective host defense against Mycobacterium tuberculosis requires the induction of Th1 cytokine responses. We investigated the regulated expression and functional role of the inducible costimulator (ICOS), a receptor known to regulate Th cytokine production, in the context of human tuberculosis. Patients with active disease, classified as high responder (HR) or low responder (LR) patients according to their in vitro T cell responses against the Ag, were evaluated for T cell expression of ICOS after M.tuberculosis-stimulation. We found that ICOS expression significantly correlated with IFN-g production by tuberculosis patients. ICOS expression levels were regulated in HR patients by Th cytokines: Th1 cytokines increased ICOS levels, whereas Th2-polarizing conditions down-regulated ICOS in these individuals. Besides, in human polarized Th cells, engagement of ICOS increased M. tuberculosis IFN-g production with a magnitude proportional to ICOS levels on those cells. Moreover, ICOS ligation augmented Ag-specific secretion of the Th1 cytokine IFN- from responsive individuals. In contrast, neither Th1 nor Th2 cytokines dramatically affected ICOS levels on Ag-stimulated T cells from LR patients, and ICOS activation did not enhance IFN-g production. However, simultaneous activation of ICOS and CD3 slightly augmented IFN-g secretion by LR patients. Together, our data suggest that the regulation of ICOS expression depends primarily on the response of T cells from tuberculosis patients to the specific Ag. IFN-g released by M. tuberculosis-specific T cells modulates ICOS levels, and accordingly, ICOS ligation induces IFN-g secretion. Thus, ICOS activation may promote the induction of protective Th1 cytokine responses to intracellular bacterial pathogens.
Fil: Quiroga, María Florencia. Universidad Abierta Interamericana. Facultad de Medicina. Cátedra de Microbiología Parasitología E Inmunología; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín. Laboratorio de Inmunogenética; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Pasquinelli, Virginia. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín. Laboratorio de Inmunogenética; Argentina. Universidad Abierta Interamericana. Facultad de Medicina. Cátedra de Microbiología Parasitología E Inmunología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Martínez, Gustavo J.. Universidad Abierta Interamericana. Facultad de Medicina. Cátedra de Microbiología Parasitología E Inmunología; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín. Laboratorio de Inmunogenética; Argentina
Fil: Jurado, Javier Oscar. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín. Laboratorio de Inmunogenética; Argentina. Universidad Abierta Interamericana. Facultad de Medicina. Cátedra de Microbiología Parasitología E Inmunología; Argentina
Fil: Zorrilla, Liliana Castro. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología. Cátedra de Microbiología, Parasitología e Inmunología; Argentina
Fil: Musella, Rosa María. Gobierno de la Ciudad de Buenos Aires. Hospital de Infecciosas "Dr. Francisco Javier Muñiz"; Argentina
Fil: Abbate, Eduardo José. Gobierno de la Ciudad de Buenos Aires. Hospital de Infecciosas "Dr. Francisco Javier Muñiz"; Argentina
Fil: Sieling, Peter A.. University of California; Estados Unidos
Fil: García, Verónica Edith. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín. Laboratorio de Inmunogenética; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Abierta Interamericana. Facultad de Medicina. Cátedra de Microbiología Parasitología E Inmunología; Argentina
Materia
TUBERCULOSIS
ICOS
COSTIMULATION
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:11336/100527
Acceder
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repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Inducible Costimulator: A Modulator of IFN-γ Production in Human TuberculosisQuiroga, María FlorenciaPasquinelli, VirginiaMartínez, Gustavo J.Jurado, Javier OscarZorrilla, Liliana CastroMusella, Rosa MaríaAbbate, Eduardo JoséSieling, Peter A.García, Verónica EdithTUBERCULOSISICOSCOSTIMULATIONhttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Effective host defense against Mycobacterium tuberculosis requires the induction of Th1 cytokine responses. We investigated the regulated expression and functional role of the inducible costimulator (ICOS), a receptor known to regulate Th cytokine production, in the context of human tuberculosis. Patients with active disease, classified as high responder (HR) or low responder (LR) patients according to their in vitro T cell responses against the Ag, were evaluated for T cell expression of ICOS after M.tuberculosis-stimulation. We found that ICOS expression significantly correlated with IFN-g production by tuberculosis patients. ICOS expression levels were regulated in HR patients by Th cytokines: Th1 cytokines increased ICOS levels, whereas Th2-polarizing conditions down-regulated ICOS in these individuals. Besides, in human polarized Th cells, engagement of ICOS increased M. tuberculosis IFN-g production with a magnitude proportional to ICOS levels on those cells. Moreover, ICOS ligation augmented Ag-specific secretion of the Th1 cytokine IFN- from responsive individuals. In contrast, neither Th1 nor Th2 cytokines dramatically affected ICOS levels on Ag-stimulated T cells from LR patients, and ICOS activation did not enhance IFN-g production. However, simultaneous activation of ICOS and CD3 slightly augmented IFN-g secretion by LR patients. Together, our data suggest that the regulation of ICOS expression depends primarily on the response of T cells from tuberculosis patients to the specific Ag. IFN-g released by M. tuberculosis-specific T cells modulates ICOS levels, and accordingly, ICOS ligation induces IFN-g secretion. Thus, ICOS activation may promote the induction of protective Th1 cytokine responses to intracellular bacterial pathogens.Fil: Quiroga, María Florencia. Universidad Abierta Interamericana. Facultad de Medicina. Cátedra de Microbiología Parasitología E Inmunología; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín. Laboratorio de Inmunogenética; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Pasquinelli, Virginia. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín. Laboratorio de Inmunogenética; Argentina. Universidad Abierta Interamericana. Facultad de Medicina. Cátedra de Microbiología Parasitología E Inmunología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Martínez, Gustavo J.. Universidad Abierta Interamericana. Facultad de Medicina. Cátedra de Microbiología Parasitología E Inmunología; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín. Laboratorio de Inmunogenética; ArgentinaFil: Jurado, Javier Oscar. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín. Laboratorio de Inmunogenética; Argentina. Universidad Abierta Interamericana. Facultad de Medicina. Cátedra de Microbiología Parasitología E Inmunología; ArgentinaFil: Zorrilla, Liliana Castro. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología. Cátedra de Microbiología, Parasitología e Inmunología; ArgentinaFil: Musella, Rosa María. Gobierno de la Ciudad de Buenos Aires. Hospital de Infecciosas "Dr. Francisco Javier Muñiz"; ArgentinaFil: Abbate, Eduardo José. Gobierno de la Ciudad de Buenos Aires. Hospital de Infecciosas "Dr. Francisco Javier Muñiz"; ArgentinaFil: Sieling, Peter A.. University of California; Estados UnidosFil: García, Verónica Edith. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín. Laboratorio de Inmunogenética; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Abierta Interamericana. Facultad de Medicina. Cátedra de Microbiología Parasitología E Inmunología; ArgentinaAmerican Association of Immunologists2006-05info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/100527Quiroga, María Florencia; Pasquinelli, Virginia; Martínez, Gustavo J.; Jurado, Javier Oscar; Zorrilla, Liliana Castro; et al.; Inducible Costimulator: A Modulator of IFN-γ Production in Human Tuberculosis; American Association of Immunologists; Journal of Immunology; 176; 10; 5-2006; 5965-59740022-1767CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.4049/jimmunol.176.10.5965info:eu-repo/semantics/altIdentifier/url/https://www.jimmunol.org/content/176/10/5965info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T10:03:29Zoai:ri.conicet.gov.ar:11336/100527instacron: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 10:03:30.262CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Inducible Costimulator: A Modulator of IFN-γ Production in Human Tuberculosis
title Inducible Costimulator: A Modulator of IFN-γ Production in Human Tuberculosis
spellingShingle Inducible Costimulator: A Modulator of IFN-γ Production in Human Tuberculosis
Quiroga, María Florencia
TUBERCULOSIS
ICOS
COSTIMULATION
title_short Inducible Costimulator: A Modulator of IFN-γ Production in Human Tuberculosis
title_full Inducible Costimulator: A Modulator of IFN-γ Production in Human Tuberculosis
title_fullStr Inducible Costimulator: A Modulator of IFN-γ Production in Human Tuberculosis
title_full_unstemmed Inducible Costimulator: A Modulator of IFN-γ Production in Human Tuberculosis
title_sort Inducible Costimulator: A Modulator of IFN-γ Production in Human Tuberculosis
dc.creator.none.fl_str_mv Quiroga, María Florencia
Pasquinelli, Virginia
Martínez, Gustavo J.
Jurado, Javier Oscar
Zorrilla, Liliana Castro
Musella, Rosa María
Abbate, Eduardo José
Sieling, Peter A.
García, Verónica Edith
author Quiroga, María Florencia
author_facet Quiroga, María Florencia
Pasquinelli, Virginia
Martínez, Gustavo J.
Jurado, Javier Oscar
Zorrilla, Liliana Castro
Musella, Rosa María
Abbate, Eduardo José
Sieling, Peter A.
García, Verónica Edith
author_role author
author2 Pasquinelli, Virginia
Martínez, Gustavo J.
Jurado, Javier Oscar
Zorrilla, Liliana Castro
Musella, Rosa María
Abbate, Eduardo José
Sieling, Peter A.
García, Verónica Edith
author2_role author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv TUBERCULOSIS
ICOS
COSTIMULATION
topic TUBERCULOSIS
ICOS
COSTIMULATION
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv Effective host defense against Mycobacterium tuberculosis requires the induction of Th1 cytokine responses. We investigated the regulated expression and functional role of the inducible costimulator (ICOS), a receptor known to regulate Th cytokine production, in the context of human tuberculosis. Patients with active disease, classified as high responder (HR) or low responder (LR) patients according to their in vitro T cell responses against the Ag, were evaluated for T cell expression of ICOS after M.tuberculosis-stimulation. We found that ICOS expression significantly correlated with IFN-g production by tuberculosis patients. ICOS expression levels were regulated in HR patients by Th cytokines: Th1 cytokines increased ICOS levels, whereas Th2-polarizing conditions down-regulated ICOS in these individuals. Besides, in human polarized Th cells, engagement of ICOS increased M. tuberculosis IFN-g production with a magnitude proportional to ICOS levels on those cells. Moreover, ICOS ligation augmented Ag-specific secretion of the Th1 cytokine IFN- from responsive individuals. In contrast, neither Th1 nor Th2 cytokines dramatically affected ICOS levels on Ag-stimulated T cells from LR patients, and ICOS activation did not enhance IFN-g production. However, simultaneous activation of ICOS and CD3 slightly augmented IFN-g secretion by LR patients. Together, our data suggest that the regulation of ICOS expression depends primarily on the response of T cells from tuberculosis patients to the specific Ag. IFN-g released by M. tuberculosis-specific T cells modulates ICOS levels, and accordingly, ICOS ligation induces IFN-g secretion. Thus, ICOS activation may promote the induction of protective Th1 cytokine responses to intracellular bacterial pathogens.
Fil: Quiroga, María Florencia. Universidad Abierta Interamericana. Facultad de Medicina. Cátedra de Microbiología Parasitología E Inmunología; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín. Laboratorio de Inmunogenética; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Pasquinelli, Virginia. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín. Laboratorio de Inmunogenética; Argentina. Universidad Abierta Interamericana. Facultad de Medicina. Cátedra de Microbiología Parasitología E Inmunología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Martínez, Gustavo J.. Universidad Abierta Interamericana. Facultad de Medicina. Cátedra de Microbiología Parasitología E Inmunología; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín. Laboratorio de Inmunogenética; Argentina
Fil: Jurado, Javier Oscar. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín. Laboratorio de Inmunogenética; Argentina. Universidad Abierta Interamericana. Facultad de Medicina. Cátedra de Microbiología Parasitología E Inmunología; Argentina
Fil: Zorrilla, Liliana Castro. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología. Cátedra de Microbiología, Parasitología e Inmunología; Argentina
Fil: Musella, Rosa María. Gobierno de la Ciudad de Buenos Aires. Hospital de Infecciosas "Dr. Francisco Javier Muñiz"; Argentina
Fil: Abbate, Eduardo José. Gobierno de la Ciudad de Buenos Aires. Hospital de Infecciosas "Dr. Francisco Javier Muñiz"; Argentina
Fil: Sieling, Peter A.. University of California; Estados Unidos
Fil: García, Verónica Edith. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín. Laboratorio de Inmunogenética; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Abierta Interamericana. Facultad de Medicina. Cátedra de Microbiología Parasitología E Inmunología; Argentina
description Effective host defense against Mycobacterium tuberculosis requires the induction of Th1 cytokine responses. We investigated the regulated expression and functional role of the inducible costimulator (ICOS), a receptor known to regulate Th cytokine production, in the context of human tuberculosis. Patients with active disease, classified as high responder (HR) or low responder (LR) patients according to their in vitro T cell responses against the Ag, were evaluated for T cell expression of ICOS after M.tuberculosis-stimulation. We found that ICOS expression significantly correlated with IFN-g production by tuberculosis patients. ICOS expression levels were regulated in HR patients by Th cytokines: Th1 cytokines increased ICOS levels, whereas Th2-polarizing conditions down-regulated ICOS in these individuals. Besides, in human polarized Th cells, engagement of ICOS increased M. tuberculosis IFN-g production with a magnitude proportional to ICOS levels on those cells. Moreover, ICOS ligation augmented Ag-specific secretion of the Th1 cytokine IFN- from responsive individuals. In contrast, neither Th1 nor Th2 cytokines dramatically affected ICOS levels on Ag-stimulated T cells from LR patients, and ICOS activation did not enhance IFN-g production. However, simultaneous activation of ICOS and CD3 slightly augmented IFN-g secretion by LR patients. Together, our data suggest that the regulation of ICOS expression depends primarily on the response of T cells from tuberculosis patients to the specific Ag. IFN-g released by M. tuberculosis-specific T cells modulates ICOS levels, and accordingly, ICOS ligation induces IFN-g secretion. Thus, ICOS activation may promote the induction of protective Th1 cytokine responses to intracellular bacterial pathogens.
publishDate 2006
dc.date.none.fl_str_mv 2006-05
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/11336/100527
Quiroga, María Florencia; Pasquinelli, Virginia; Martínez, Gustavo J.; Jurado, Javier Oscar; Zorrilla, Liliana Castro; et al.; Inducible Costimulator: A Modulator of IFN-γ Production in Human Tuberculosis; American Association of Immunologists; Journal of Immunology; 176; 10; 5-2006; 5965-5974
0022-1767
CONICET Digital
CONICET
url http://hdl.handle.net/11336/100527
identifier_str_mv Quiroga, María Florencia; Pasquinelli, Virginia; Martínez, Gustavo J.; Jurado, Javier Oscar; Zorrilla, Liliana Castro; et al.; Inducible Costimulator: A Modulator of IFN-γ Production in Human Tuberculosis; American Association of Immunologists; Journal of Immunology; 176; 10; 5-2006; 5965-5974
0022-1767
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.4049/jimmunol.176.10.5965
info:eu-repo/semantics/altIdentifier/url/https://www.jimmunol.org/content/176/10/5965
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
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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
application/pdf
application/pdf
application/pdf
application/pdf
dc.publisher.none.fl_str_mv American Association of Immunologists
publisher.none.fl_str_mv American Association of Immunologists
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
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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score 13.070432

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