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Your search keyword '"Javier Oscar Jurado"' showing total 2 results
Start Over Author "Javier Oscar Jurado" Journal the journal of immunology
2 results on '"Javier Oscar Jurado"'

1. Programmed Death (PD)-1:PD-Ligand 1/PD-Ligand 2 Pathway Inhibits T Cell Effector Functions during Human Tuberculosis

Author

María Florencia Quiroga, Virginia Pasquinelli, Javier Oscar Jurado, Eduardo Abbate, Rosa M. Musella, H. Eduardo Chuluyan, Gustavo J. Martinez, Ivana Belén Alvarez, and Verónica E. García

Subjects
CIENCIAS MÉDICAS Y DE LA SALUD, Programmed Cell Death 1 Ligand 2 Protein, T-Lymphocytes, CD3, T cell, Programmed Cell Death 1 Receptor, Immunology, Inmunología, Receptors, Cell Surface, CITOQUINAS, Biology, Lymphocyte Activation, TUBERCULOSIS, B7-H1 Antigen, Mycobacterium tuberculosis, Interferon-gamma, Immune system, Signaling lymphocytic activation molecule, Signaling Lymphocytic Activation Molecule Family Member 1, Antigens, CD, medicine, Humans, Tuberculosis, Immunology and Allergy, Antigens, Cells, Cultured, biology.organism_classification, Cell biology, PD1, Medicina Básica, medicine.anatomical_structure, biology.protein, Intercellular Signaling Peptides and Proteins, Apoptosis Regulatory Proteins, CD8, Protein Binding, Signal Transduction
Abstract

Protective immunity against Mycobacterium tuberculosis requires the generation of cell-mediated immunity. We investigated the expression and role of programmed death 1 (PD-1) and its ligands, molecules known to modulate T cell activation, in the regulation of IFN-γ production and lytic degranulation during human tuberculosis. We demonstrated that specific Ag-stimulation increased CD3+PD-1+ lymphocytes in peripheral blood and pleural fluid from tuberculosis patients in direct correlation with IFN-γ production from these individuals. Moreover, M. tuberculosis-induced IFN-γ participated in the up-regulation of PD-1 expression. Blockage of PD-1 or PD-1 and its ligands (PD-Ls: PD-L1, PD-L2) enhanced the specific degranulation of CD8+ T cells and the percentage, of specific IFN-γ-producing lymphocytes against the pathogen, demonstrating that the PD-1:PD-Ls pathway inhibits T cell effector functions during active M. tuberculosis infection. Furthermore, the simultaneous blockage of the inhibitory receptor PD-1 together with the activation of the costimulatory protein signaling lymphocytic activation molecule led to the promotion of protective IFN-γ responses to M. tuberculosis, even in patients with weak cell-mediated immunity against the bacteria. Together, we demonstrated that PD-1 interferes with T cell effector functions against M. tuberculosis, suggesting that PD-1 has a key regulatory role during the immune response of the host to the pathogen. Fil: Jurado, Javier Oscar. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina Fil: Alvarez, Ivana Belén. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica; Argentina Fil: Pasquinelli, Virginia. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina Fil: Martínez, Gustavo J.. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina Fil: Quiroga, María F.. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina Fil: Abbate, Eduardo. Gobierno de la Ciudad de Buenos Airs. Hospital de Infecciosas "F. Muñiz"; Argentina Fil: Musella, Rosa María. Gobierno de la Ciudad de Buenos Airs. Hospital de Infecciosas "F. Muñiz"; Argentina Fil: Chuluyan, Hector Eduardo. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: 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; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina

Published
2008

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

Author

Javier Oscar Jurado, Virginia Pasquinelli, Peter A. Sieling, María Florencia Quiroga, Rosa M. Musella, Eduardo José Abbate, Liliana Castro Zorrilla, Verónica E. García, and Gustavo J. Martinez

Subjects
Antigens, Differentiation, T-Lymphocyte, Intracellular Fluid, CD3, medicine.medical_treatment, T cell, Immunology, Context (language use), TUBERCULOSIS, Ligands, Cell Line, Ciencias Biológicas, Inducible T-Cell Co-Stimulator Protein, COSTIMULATION, Interferon-gamma, Biología Celular, Microbiología, Antigen, medicine, Humans, Immunology and Allergy, Secretion, Receptor, Tuberculosis, Pulmonary, Cells, Cultured, biology, Antibodies, Monoclonal, T-Lymphocytes, Helper-Inducer, Th1 Cells, Cytokine, medicine.anatomical_structure, ICOS, Gene Expression Regulation, biology.protein, CIENCIAS NATURALES Y EXACTAS
Abstract

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

Published
2006

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