pf-3512676 and Disease-Models--Animal

pf-3512676 has been researched along with Disease-Models--Animal* in 1 studies

Other Studies

1 other study(ies) available for pf-3512676 and Disease-Models--Animal

Article	Year
Pulmonary mucosal immunity mediated through CpG provides adequate protection against pulmonary Mycobacterium tuberculosis infection in the mouse model. A role for type I interferon. Tuberculosis (Edinburgh, Scotland), 2020, Volume: 123 Toll-Like Receptor (TLR) 9 stimulation is required for induction of potent immune responses against pathogen invasion. The use of unmethylated CpG as adjuvants in vaccines provides an excellent means of stimulating adaptive immunity. Our data demonstrate that CpG-C provided prolonged immune responses in the mouse model of tuberculosis when formulated with liposomes and the Mycobacterium tuberculosis antigen ESAT-6. A reduction in the mycobacterial burden was best achieved when administered as an intranasal vaccine and was dependent on type I interferon (IFN). There was a significant difference between CpG-C inoculated wild type and IFN-αR1 Topics: Adjuvants, Immunologic; Administration, Intranasal; Animals; Antigens, Bacterial; Bacterial Proteins; Cells, Cultured; Disease Models, Animal; Female; Host-Pathogen Interactions; Immunity, Mucosal; Interferon-gamma; Lung; Mice, Inbred C57BL; Mice, Knockout; Mycobacterium tuberculosis; Myeloid Differentiation Factor 88; Nasal Sprays; Oligodeoxyribonucleotides; Receptor, Interferon alpha-beta; Respiratory Mucosa; Signal Transduction; Toll-Like Receptor 9; Tuberculosis Vaccines; Tuberculosis, Pulmonary	2020

Article

Year

Pulmonary mucosal immunity mediated through CpG provides adequate protection against pulmonary Mycobacterium tuberculosis infection in the mouse model. A role for type I interferon.

Tuberculosis (Edinburgh, Scotland), 2020, Volume: 123

Toll-Like Receptor (TLR) 9 stimulation is required for induction of potent immune responses against pathogen invasion. The use of unmethylated CpG as adjuvants in vaccines provides an excellent means of stimulating adaptive immunity. Our data demonstrate that CpG-C provided prolonged immune responses in the mouse model of tuberculosis when formulated with liposomes and the Mycobacterium tuberculosis antigen ESAT-6. A reduction in the mycobacterial burden was best achieved when administered as an intranasal vaccine and was dependent on type I interferon (IFN). There was a significant difference between CpG-C inoculated wild type and IFN-αR1

Topics: Adjuvants, Immunologic; Administration, Intranasal; Animals; Antigens, Bacterial; Bacterial Proteins; Cells, Cultured; Disease Models, Animal; Female; Host-Pathogen Interactions; Immunity, Mucosal; Interferon-gamma; Lung; Mice, Inbred C57BL; Mice, Knockout; Mycobacterium tuberculosis; Myeloid Differentiation Factor 88; Nasal Sprays; Oligodeoxyribonucleotides; Receptor, Interferon alpha-beta; Respiratory Mucosa; Signal Transduction; Toll-Like Receptor 9; Tuberculosis Vaccines; Tuberculosis, Pulmonary

2020