Programmed death-1 (PD-1)-deficient mice are extraordinarily sensitive to tuberculosis. - Wikidata - wikimedia - TriplyDB

Programmed death-1 (PD-1)-deficient mice are extraordinarily sensitive to tuberculosis.

Programmed death-1 (PD-1)-deficient mice are extraordinarily sensitive to tuberculosis.

http://www.wikidata.org/entity/Q34067889

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Th1 and Th17 Cells in Tuberculosis: Protection, Pathology, and Biomarkers Novel adjunctive therapies for the treatment of tuberculosis Herpesvirus exploitation of host immune inhibitory pathways Adjunct Strategies for Tuberculosis Vaccines: Modulating Key Immune Cell Regulatory Mechanisms to Potentiate Vaccination PD-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 Treatment Both 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 inhibition T cells from Programmed Death-1 deficient mice respond poorly to Mycobacterium tuberculosis infection Phosphorylated STAT3 and PD-1 regulate IL-17 production and IL-23 receptor expression in Mycobacterium tuberculosis infection Programmed 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 mice Orchestration 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 tuberculosis PD-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 tuberculosis Programmed death ligand 1 is over-expressed by neutrophils in the blood of patients with active tuberculosis Regulation of neutrophils by interferon-γ limits lung inflammation during tuberculosis infection.Initiation and regulation of T-cell responses in tuberculosis ICOS 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 disease Interleukin 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 virulence HIV 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 Disease CD4 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

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P2860

Programmed death-1 (PD-1)-deficient mice are extraordinarily sensitive to tuberculosis.

http://www.wikidata.org/entity/Q34067889

description

2010 nî lūn-bûn

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2010 թուականի Յուլիսին հրատարակուած գիտական յօդուած

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2010 թվականի հուլիսին հրատարակված գիտական հոդված

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2010年の論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年论文

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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

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PNAS.1007394107

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Proceedings of the National Academy of Sciences of the United States of America

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Programmed death-1 (PD-1)-deficient mice are extraordinarily sensitive to tuberculosis.

@en

P2093

Bing Chen

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Emilie J Wang

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Eszter Lázár-Molnár

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Juan Lin

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Kari A Sweeney

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Stanley G Nathenson

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Steven C Almo

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Weijun Liu

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William R Jacobs

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P2860

Blockade of endogenous B7-H1 suppresses antibacterial protection after primary Listeria monocytogenes infection

Engagement of the PD-1 immunoinhibitory receptor by a novel B7 family member leads to negative regulation of lymphocyte activation

Development of lupus-like autoimmune diseases by disruption of the PD-1 gene encoding an ITIM motif-carrying immunoreceptor

PD-L2 is a second ligand for PD-1 and inhibits T cell activation

The B7 family revisited

Restoring function in exhausted CD8 T cells during chronic viral infection

Immunology of tuberculosis

PD-1 expression on HIV-specific T cells is associated with T-cell exhaustion and disease progression

Tumor necrosis factor-alpha is required in the protective immune response against Mycobacterium tuberculosis in mice

PD-1 immunoreceptor inhibits B cell receptor-mediated signaling by recruiting src homology 2-domain-containing tyrosine phosphatase 2 to phosphotyrosine.

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13402-13407

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10.1073/PNAS.1007394107

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30

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107

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Steven A Porcelli

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2010-07-12T00:00:00Z

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45167374

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20624978

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Akafuba bulwadde

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2922129

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