PD-1 blockage reverses immune dysfunction and hepatitis B viral persistence in a mouse animal model. - Wikidata - awgldk - TriplyDB

PD-1 blockage reverses immune dysfunction and hepatitis B viral persistence in a mouse animal model.

PD-1 blockage reverses immune dysfunction and hepatitis B viral persistence in a mouse animal model.

http://www.wikidata.org/entity/Q34325908

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Analysis of peripheral blood dendritic cells as a non-invasive tool in the follow-up of patients with chronic hepatitis C Specific CD8(+) T cell response immunotherapy for hepatocellular carcinoma and viral hepatitis T-cell exhaustion in chronic hepatitis B infection: current knowledge and clinical significance Hepatitis B Virus Immunopathology, Model Systems, and Current Therapies Cancer immunotherapy by targeting immune checkpoints: mechanism of T cell dysfunction in cancer immunity and new therapeutic targets.PD1 is highly expressed in diffuse large B-cell lymphoma with hepatitis B virus infection.Tumor necrosis factor-alpha induced by hepatitis B virus core mediating the immune response for hepatitis B viral clearance in mice model Chronic thoracic spinal cord injury impairs CD8+ T-cell function by up-regulating programmed cell death-1 expression.Hepatitis B virus: new therapeutic perspectives.The hepatitis B virus-associated tumor microenvironment in hepatocellular carcinoma.microRNA-4717 differentially interacts with its polymorphic target in the PD1 3' untranslated region: A mechanism for regulating PD-1 expression and function in HBV-associated liver diseases.Present and future therapies of hepatitis B: From discovery to cure PD-1 Blunts the Function of Ovarian Tumor-Infiltrating Dendritic Cells by Inactivating NF-κB Chronic hepatitis B: what should be the goal for new therapies?Clearing Persistent Extracellular Antigen of Hepatitis B Virus: An Immunomodulatory Strategy To Reverse Tolerance for an Effective Therapeutic Vaccination Maternal-Derived Hepatitis B Virus e Antigen Alters Macrophage Function in Offspring to Drive Viral Persistence after Vertical Transmission.Interferon-γ facilitates hepatic antiviral T cell retention for the maintenance of liver-induced systemic tolerance.Blockade of the negative co-stimulatory molecules PD-1 and CTLA-4 improves survival in primary and secondary fungal sepsis.Altered Maturation Status and Possible Immune Exhaustion of CD8 T Lymphocytes in the Peripheral Blood of Patients Presenting With Acute Coronary Syndromes.Immune targeting of PD-1(hi) expressing cells during and after antiretroviral therapy in SIV-infected rhesus macaques.The expression of programmed death-1 in circulating CD4+ and CD8+ T cells during hepatitis B virus infection progression and its correlation with clinical baseline characteristics.Immunocompetent nontransgenic mouse models for studying hepatitis B virus immune responses.How to achieve immune control in chronic hepatitis B?Modeling hepatitis B virus infection, immunopathology and therapy in mice.Chronic hepatitis B: A wave of new therapies on the horizon.Immunotherapy in hepatocellular carcinoma: Primed to make a difference?Review article: novel therapies for hepatitis B virus cure - advances and perspectives.Novel targets for hepatitis B virus therapy.Immune Evasion Strategies during Chronic Hepatitis B and C Virus Infection Hepatitis B core antigen upregulates B7-H1 on dendritic cells by activating the AKT/ERK/P38 pathway: a possible mechanism of hepatitis B virus persistence.HIV-hepatitis B virus co-infection: epidemiology, pathogenesis, and treatment.Mechanisms of Hepatitis B Virus Persistence.Cure Strategies for Hepatitis B Virus: The Promise of Immunotherapy.Complementary Effects of Interleukin-15 and Alpha Interferon Induce Immunity in Hepatitis B Virus Transgenic Mice.Molecular mechanisms of HBeAg in persistent HBV infection.Induction of Multiple Immune Regulatory Pathways with Differential Impact in HCV/HIV Coinfection.Telomere Dynamics in Immune Senescence and Exhaustion Triggered by Chronic Viral Infection.Hepatitis B cure: From discovery to regulatory approval.HBV Core Protein Enhances Cytokine Production.Therapeutic recovery of hepatitis B virus (HBV)-induced hepatocyte-intrinsic immune defect reverses systemic adaptive immune tolerance.

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PD-1 blockage reverses immune dysfunction and hepatitis B viral persistence in a mouse animal model.

http://www.wikidata.org/entity/Q34325908

description

2012 nî lūn-bûn

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2012 թուականի Յունիսին հրատարակուած գիտական յօդուած

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2012年の論文

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2012年論文

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2012年論文

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2012年論文

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2012年论文

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Horng-Tay Tzeng

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Hsiu-Jung Liao

http://www.w3.org/2001/XMLSchema#string

Hwei-Fang Tsai

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Lieping Chen

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Pei-Jer Chen

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Ping-Ning Hsu

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Yi-Jiun Lin

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P2860

Induced expression of PD-1, a novel member of the immunoglobulin gene superfamily, upon programmed cell death

Upregulation of PD-1 Expression on Circulating and Intrahepatic Hepatitis C Virus-Specific CD8+ T Cells Associated with Reversible Immune Dysfunction

Restoring function in exhausted CD8 T cells during chronic viral infection

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

Immune effectors required for hepatitis B virus clearance

Hepatitis B virus core antigen determines viral persistence in a C57BL/6 mouse model.

Hydrodynamic injection of viral DNA: a mouse model of acute hepatitis B virus infection

PD-1 inhibits antiviral immunity at the effector phase in the liver.

Expression of the interleukin-7 receptor alpha chain (CD127) on virus-specific CD8+ T cells identifies functionally and phenotypically defined memory T cells during acute resolving hepatitis B virus infection

Immunology of hepatitis B infection.

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viral persistence

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