Programmed death 1 protects from fatal circulatory failure during systemic virus infection of mice. - Test2 - elhamkhani - TriplyDB

Programmed death 1 protects from fatal circulatory failure during systemic virus infection of mice.

Programmed death 1 protects from fatal circulatory failure during systemic virus infection of mice.

http://www.wikidata.org/entity/Q36478253

about

The protein LEM promotes CD8⁺ T cell immunity through effects on mitochondrial respiration T Lymphocyte-Endothelial Interactions: Emerging Understanding of Trafficking and Antigen-Specific Immunity Type I interferon is a therapeutic target for virus-induced lethal vascular damage.Endothelial cell dysfunction in viral hemorrhage and edema.Vitamin D increases programmed death receptor-1 expression in Crohn's disease.Interplay between regulatory T cells and PD-1 in modulating T cell exhaustion and viral control during chronic LCMV infection.Immune control and failure in HCV infection--tipping the balance.Postnatal acquisition of primary rhesus cytomegalovirus infection is associated with prolonged virus shedding and impaired CD4+ T lymphocyte function.The transcription factor FoxO1 sustains expression of the inhibitory receptor PD-1 and survival of antiviral CD8(+) T cells during chronic infection Reservoir host immune responses to emerging zoonotic viruses.Inhibitory Receptors Beyond T Cell Exhaustion.PD-L1 Expression on Retrovirus-Infected Cells Mediates Immune Escape from CD8+ T Cell Killing Genetic absence of PD-1 promotes accumulation of terminally differentiated exhausted CD8+ T cells CD4 T Cell Depletion Substantially Augments the Rescue Potential of PD-L1 Blockade for Deeply Exhausted CD8 T Cells.Chimeric Mice with Competent Hematopoietic Immunity Reproduce Key Features of Severe Lassa Fever.Programmed death-1 controls T cell survival by regulating oxidative metabolism.The Inhibitory Receptor NKG2A Sustains Virus-Specific CD8⁺ T Cells in Response to a Lethal Poxvirus Infection Potentiation of immunomodulatory antibody therapy with oncolytic viruses for treatment of cancer.PD-1 promotes immune exhaustion by inducing antiviral T cell motility paralysis 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.PSGL-1 Is an Immune Checkpoint Regulator that Promotes T Cell Exhaustion.High antigen levels induce an exhausted phenotype in a chronic infection without impairing T cell expansion and survival Inhibitory Receptor Expression Depends More Dominantly on Differentiation and Activation than "Exhaustion" of Human CD8 T Cells.Type I Interferon Impairs Specific Antibody Responses Early during Establishment of LCMV Infection.Therapeutic depletion of natural killer cells controls persistent infection.Hypoxia-inducible factors enhance the effector responses of CD8(+) T cells to persistent antigen.Molecular signatures of T-cell inhibition in HIV-1 infection.Manipulating the PD-1 pathway to improve immunity.Deciphering and reversing tumor immune suppression.Tolerance and exhaustion: defining mechanisms of T cell dysfunction.Vaccine Targeting of Subdominant CD8+ T Cell Epitopes Increases the Breadth of the T Cell Response upon Viral Challenge, but May Impair Immediate Virus Control.T cell exhaustion: from pathophysiological basics to tumor immunotherapy.Conserved Region C Functions To Regulate PD-1 Expression and Subsequent CD8 T Cell Memory.CD8 T-cell regulation by T regulatory cells and the programmed cell death protein 1 pathway.Bioenergetic Insufficiencies Due to Metabolic Alterations Regulated by the Inhibitory Receptor PD-1 Are an Early Driver of CD8(+) T Cell Exhaustion.Differential Inhibitory Receptor Expression on T Cells Delineates Functional Capacities in Chronic Viral Infection.Host genetics play a critical role in controlling CD8 T cell function and lethal immunopathology during chronic viral infection.Innate and Adaptive Immune Responses in Chronic HCV Infection.T cell exhaustion: a means or an end?

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Programmed death 1 protects from fatal circulatory failure during systemic virus infection of mice.

http://www.wikidata.org/entity/Q36478253

description

2012 nî lūn-bûn

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2012年学术文章

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Programmed death 1 protects fr ...... temic virus infection of mice.

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Journal of Experimental Medicine

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Programmed death 1 protects fr ...... stemic virus infection of mice

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Carsten A Wagner

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Dominique Loffing-Cueni

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Helge Frebel

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Johannes Vogel

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Kirsten Richter

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Michael Kurrer

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Thomas Braunschweiler

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Veronika Nindl

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P2860

Safety, activity, and immune correlates of anti-PD-1 antibody in cancer

The PD-1 pathway in tolerance and autoimmunity

Murine Model for Dengue Virus-Induced Lethal Disease with Increased Vascular Permeability

Synergistic Reversal of Intrahepatic HCV-Specific CD8 T Cell Exhaustion by Combined PD-1/CTLA-4 Blockade

Safety and Activity of Anti–PD-L1 Antibody in Patients with Advanced Cancer

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

Autoimmune dilated cardiomyopathy in PD-1 receptor-deficient mice

Restoring function in exhausted CD8 T cells during chronic viral infection

Phenotypic analysis of antigen-specific T lymphocytes

Cytotoxicity mediated by T cells and natural killer cells is greatly impaired in perforin-deficient mice

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2485-2499

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scholarly article

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10.1084/JEM.20121015

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13

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209

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Reto A Schuepbach

Annette Oxenius

Burkhard Ludewig

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2012-12-10T00:00:00Z

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233892553

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23230000

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3526355

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