Histone deacetylase inhibitors impair the elimination of HIV-infected cells by cytotoxic T-lymphocytes - Wikidata - thesis-toulmin - TriplyDB

Histone deacetylase inhibitors impair the elimination of HIV-infected cells by cytotoxic T-lymphocytes

Histone deacetylase inhibitors impair the elimination of HIV-infected cells by cytotoxic T-lymphocytes

http://www.wikidata.org/entity/Q27324527

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Targeting the latent reservoir to achieve functional HIV cure Animal Models for HIV Cure Research Controlling HIV-1: Non-Coding RNA Gene Therapy Approaches to a Functional Cure Challenges and Opportunities for T-Cell-Mediated Strategies to Eliminate HIV Reservoirs Manipulation of the host protein acetylation network by human immunodeficiency virus type 1 Multi-dose Romidepsin Reactivates Replication Competent SIV in Post-antiretroviral Rhesus Macaque Controllers Achieving HIV-1 Control through RNA-Directed Gene Regulation Latency reversal and viral clearance to cure HIV-1.A Subset of Latency-Reversing Agents Expose HIV-Infected Resting CD4+ T-Cells to Recognition by Cytotoxic T-Lymphocytes.Similarity in viral and host promoters couples viral reactivation with host cell migration Promoter Targeting RNAs: Unexpected Contributors to the Control of HIV-1 Transcription.Ex vivo analysis identifies effective HIV-1 latency-reversing drug combinations.The Depsipeptide Romidepsin Reverses HIV-1 Latency In Vivo Expanded cytotoxic T-cell lymphocytes target the latent HIV reservoir Reactivation Kinetics of HIV-1 and Susceptibility of Reactivated Latently Infected CD4+ T Cells to HIV-1-Specific CD8+ T Cells.Human Galectin-9 Is a Potent Mediator of HIV Transcription and Reactivation Innate Immune Activity Correlates with CD4 T Cell-Associated HIV-1 DNA Decline during Latency-Reversing Treatment with Panobinostat.Histone Deacetylase Inhibitors Enhance CD4 T Cell Susceptibility to NK Cell Killing but Reduce NK Cell Function.HIV persistence in the setting of antiretroviral therapy: when, where and how does HIV hide?Synergistic Activation of Latent HIV-1 Expression by Novel Histone Deacetylase Inhibitors and Bryostatin-1.The effect of Ingenol-B on the suppressive capacity of elite suppressor HIV-specific CD8+ T cells.HIV-specific CD8⁺ T cells and HIV eradication Towards HIV-1 remission: potential roles for broadly neutralizing antibodies.Recent developments in the effort to cure HIV infection: going beyond N = 1.Sequential treatment with 5-aza-2'-deoxycytidine and deacetylase inhibitors reactivates HIV-1.Gnidimacrin, a Potent Anti-HIV Diterpene, Can Eliminate Latent HIV-1 Ex Vivo by Activation of Protein Kinase C β.A Subset of CD4/CD8 Double-Negative T Cells Expresses HIV Proteins in Patients on Antiretroviral Therapy.The Effect of Latency Reversal Agents on Primary CD8+ T Cells: Implications for Shock and Kill Strategies for Human Immunodeficiency Virus Eradication.Biphasic CD8+ T-Cell Defense in Simian Immunodeficiency Virus Control by Acute-Phase Passive Neutralizing Antibody Immunization.Highlights from the Keystone Symposium on HIV Persistence 2015: 26-30 April 2015, Boston, Massachusetts, USA The differential short- and long-term effects of HIV-1 latency-reversing agents on T cell function Short-term administration of disulfiram for reversal of latent HIV infection: a phase 2 dose-escalation study.Impact of the microbial derived short chain fatty acid propionate on host susceptibility to bacterial and fungal infections in vivo.In vitro effects of the small-molecule protein kinase C agonists on HIV latency reactivation.HIV-1 Latency and Eradication: Past, Present and Future International AIDS Society global scientific strategy: towards an HIV cure 2016.HIV eradication: combinatorial approaches to activate latent viruses.Landscape review of current HIV 'kick and kill' cure research - some kicking, not enough killing.Histone deacetylase inhibitors as immunomodulators in cancer therapeutics.Kill: boosting HIV-specific immune responses.

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Histone deacetylase inhibitors impair the elimination of HIV-infected cells by cytotoxic T-lymphocytes

http://www.wikidata.org/entity/Q27324527

description

2014 nî lūn-bûn

@nan

2014 թուականի Օգոստոսին հրատարակուած գիտական յօդուած

@hyw

2014 թվականի օգոստոսին հրատարակված գիտական հոդված

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2014年の論文

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2014年論文

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2014年論文

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2014年論文

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2014年論文

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2014年論文

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2014年论文

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Histone deacetylase inhibitors ...... lls by cytotoxic T-lymphocytes

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Histone deacetylase inhibitors ...... lls by cytotoxic T-lymphocytes

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Histone deacetylase inhibitors ...... lls by cytotoxic T-lymphocytes

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Histone deacetylase inhibitors ...... lls by cytotoxic T-lymphocytes

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Histone deacetylase inhibitors ...... lls by cytotoxic T-lymphocytes

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Histone deacetylase inhibitors ...... lls by cytotoxic T-lymphocytes

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Histone deacetylase inhibitors ...... lls by cytotoxic T-lymphocytes

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JOURNAL.PPAT.1004287

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Histone deacetylase inhibitors ...... lls by cytotoxic T-lymphocytes

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Colin Kovacs

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Dan Karel

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Darrell J Irvine

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Maria Foley

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Stefanie Mueller

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P2860

Histone deacetylase inhibition modulates indoleamine 2,3-dioxygenase–dependent DC functions and regulates experimental graft-versus-host disease in mice

Expression of latent HIV induced by the potent HDAC inhibitor suberoylanilide hydroxamic acid

The histone deacetylase inhibitor Trichostatin A modulates CD4+ T cell responses

High avidity CD8+ T cells efficiently eliminate motile HIV-infected targets and execute a locally focused program of anti-viral function

IL-21 in synergy with IL-15 or IL-18 enhances IFN-gamma production in human NK and T cells

Identification of a reservoir for HIV-1 in patients on highly active antiretroviral therapy

Identification of RANTES, MIP-1 alpha, and MIP-1 beta as the major HIV-suppressive factors produced by CD8+ T cells

The end of AIDS: HIV infection as a chronic disease

Histone deacetylase inhibitor romidepsin induces HIV expression in CD4 T cells from patients on suppressive antiretroviral therapy at concentrations achieved by clinical dosing.

Latent infection of CD4+ T cells provides a mechanism for lifelong persistence of HIV-1, even in patients on effective combination therapy

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Bruce D. Walker

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