Programmed death-1 (PD-1)-deficient mice are extraordinarily sensitive to tuberculosis.
about
Th1 and Th17 Cells in Tuberculosis: Protection, Pathology, and BiomarkersNovel adjunctive therapies for the treatment of tuberculosisHerpesvirus exploitation of host immune inhibitory pathwaysAdjunct Strategies for Tuberculosis Vaccines: Modulating Key Immune Cell Regulatory Mechanisms to Potentiate VaccinationPD-1, PD-L1 and PD-L2 Gene Expression on T-Cells and Natural Killer Cells Declines in Conjunction with a Reduction in PD-1 Protein during the Intensive Phase of Tuberculosis TreatmentBoth PD-1 ligands protect the kidney from ischemia reperfusion injury.CD4 T cells promote rather than control tuberculosis in the absence of PD-1-mediated inhibitionT cells from Programmed Death-1 deficient mice respond poorly to Mycobacterium tuberculosis infectionPhosphorylated STAT3 and PD-1 regulate IL-17 production and IL-23 receptor expression in Mycobacterium tuberculosis infectionProgrammed death 1 deficiency induces the polarization of macrophages/microglia to the M1 phenotype after spinal cord injury in mice.Manipulation of costimulatory molecules by intracellular pathogens: veni, vidi, vici!!Blockade of the programmed death-1 pathway restores sarcoidosis CD4(+) T-cell proliferative capacity.Foxp3+ regulatory T cells among tuberculosis patients: impact on prognosis and restoration of antigen specific IFN-γ producing T cells.Role of PPE18 protein in intracellular survival and pathogenicity of Mycobacterium tuberculosis in miceOrchestration of pulmonary T cell immunity during Mycobacterium tuberculosis infection: immunity interruptus.Involvement of CD244 in regulating CD4+ T cell immunity in patients with active tuberculosis.Immunology studies in non-human primate models of tuberculosisPD-1 suppresses protective immunity to Streptococcus pneumoniae through a B cell-intrinsic mechanism.T lymphocyte surface expression of exhaustion markers as biomarkers of the efficacy of chemotherapy for tuberculosisProgrammed death ligand 1 is over-expressed by neutrophils in the blood of patients with active tuberculosisRegulation of neutrophils by interferon-γ limits lung inflammation during tuberculosis infection.Initiation and regulation of T-cell responses in tuberculosisICOS and Bcl6-dependent pathways maintain a CD4 T cell population with memory-like properties during tuberculosis.Mechanisms of indirect acute lung injury: a novel role for the coinhibitory receptor, programmed death-1.Inhibitory Receptors Beyond T Cell Exhaustion.PD-1 Expression and Cytokine Secretion Profiles of Mycobacterium tuberculosis-Specific CD4+ T-Cell Subsets; Potential Correlates of Containment in HIV-TB Co-Infection.TIM3 Mediates T Cell Exhaustion during Mycobacterium tuberculosis Infection.IL-17 and IFN-γ expression in lymphocytes from patients with active tuberculosis correlates with the severity of the diseaseInterleukin 27R regulates CD4+ T cell phenotype and impacts protective immunity during Mycobacterium tuberculosis infection.Tuberculosis Therapy Modifies the Cytokine Profile, Maturation State, and Expression of Inhibitory Molecules on Mycobacterium tuberculosis-Specific CD4+ T-Cells.Differences in antigen-specific CD4+ responses to opportunistic infections in HIV infection.Innate IFN-γ is essential for programmed death ligand-1-mediated T cell stimulation following Listeria monocytogenes infection.Excessive Cytolytic Responses Predict Tuberculosis Relapse After Apparently Successful Treatment.Programmed death 1 protects from fatal circulatory failure during systemic virus infection of mice.PE11, a PE/PPE family protein of Mycobacterium tuberculosis is involved in cell wall remodeling and virulenceHIV Progression Perturbs the Balance of the Cell-Mediated and Anti-Inflammatory Adaptive and Innate Mycobacterial Immune Response.Mycobacteria-responsive sonic hedgehog signaling mediates programmed death-ligand 1- and prostaglandin E2-induced regulatory T cell expansion.Costimulatory and Coinhibitory Receptor Pathways in Infectious DiseaseCD4 T Cell-Derived IFN-γ Plays a Minimal Role in Control of Pulmonary Mycobacterium tuberculosis Infection and Must Be Actively Repressed by PD-1 to Prevent Lethal Disease.Evaluation of innate and adaptive immunity contributing to the antitumor effects of PD1 blockade in an orthotopic murine model of pancreatic cancer
P2860
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P2860
Programmed death-1 (PD-1)-deficient mice are extraordinarily sensitive to tuberculosis.
description
2010 nî lūn-bûn
@nan
2010 թուականի Յուլիսին հրատարակուած գիտական յօդուած
@hyw
2010 թվականի հուլիսին հրատարակված գիտական հոդված
@hy
2010年の論文
@ja
2010年論文
@yue
2010年論文
@zh-hant
2010年論文
@zh-hk
2010年論文
@zh-mo
2010年論文
@zh-tw
2010年论文
@wuu
name
Programmed death-1 (PD-1)-deficient mice are extraordinarily sensitive to tuberculosis.
@ast
Programmed death-1 (PD-1)-deficient mice are extraordinarily sensitive to tuberculosis.
@en
type
label
Programmed death-1 (PD-1)-deficient mice are extraordinarily sensitive to tuberculosis.
@ast
Programmed death-1 (PD-1)-deficient mice are extraordinarily sensitive to tuberculosis.
@en
prefLabel
Programmed death-1 (PD-1)-deficient mice are extraordinarily sensitive to tuberculosis.
@ast
Programmed death-1 (PD-1)-deficient mice are extraordinarily sensitive to tuberculosis.
@en
P2093
P2860
P356
P1476
Programmed death-1 (PD-1)-deficient mice are extraordinarily sensitive to tuberculosis.
@en
P2093
Emilie J Wang
Eszter Lázár-Molnár
Kari A Sweeney
Stanley G Nathenson
Steven C Almo
Weijun Liu
William R Jacobs
P2860
P304
13402-13407
P356
10.1073/PNAS.1007394107
P407
P577
2010-07-12T00:00:00Z