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Search Results to Ed Barker

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overview My Scopus ID is 7103411264. My NIH COMMONS name is BARKERE. Research Areas: Natural killer cells and HIV, innate lymphoid cells in HIV infection. My Faculty Profile at Rush University Medical Center: My Laboratory: My NCBI Bibliography: My Scopus: Education: PhD, University of Illinois

One or more keywords matched the following items that are connected to Barker, Ed

Item TypeName
Concept HIV Seropositivity
Concept HIV-1
Concept HIV-2
Concept HIV Envelope Protein gp120
Concept HIV
Concept HIV Core Protein p24
Concept HIV Long-Term Survivors
Concept HIV Infections
Concept Anti-HIV Agents
Academic Article Dysfunctional natural killer cells, in vivo, are governed by HIV viremia regardless of whether the infected individual is on antiretroviral therapy.
Academic Article Interferon-alpha administration enhances CD8+ T cell activation in HIV infection.
Academic Article Killing of human immunodeficiency virus-infected primary T-cell blasts by autologous natural killer cells is dependent on the ability of the virus to alter the expression of major histocompatibility complex class I molecules.
Academic Article HLA-C and HLA-E reduce antibody-dependent natural killer cell-mediated cytotoxicity of HIV-infected primary T cell blasts.
Academic Article HIV modulates the expression of ligands important in triggering natural killer cell cytotoxic responses on infected primary T-cell blasts.
Academic Article Role of natural killer cells in HIV pathogenesis.
Academic Article Lysis of endogenously infected CD4+ T cell blasts by rIL-2 activated autologous natural killer cells from HIV-infected viremic individuals.
Academic Article HIV-1 Vpr triggers natural killer cell-mediated lysis of infected cells through activation of the ATR-mediated DNA damage response.
Academic Article Degranulation of natural killer cells following interaction with HIV-1-infected cells is hindered by downmodulation of NTB-A by Vpu.
Academic Article Preparation and use of HIV-1 infected primary CD4+ T-cells as target cells in natural killer cell cytotoxic assays.
Academic Article The natural killer cell cytotoxic function is modulated by HIV-1 accessory proteins.
Academic Article Human tetherin exerts strong selection pressure on the HIV-1 group N Vpu protein.
Academic Article The natural killer cell interferon-gamma response to bacteria is diminished in untreated HIV-1 infection and defects persist despite viral suppression.
Academic Article Downmodulation of CCR7 by HIV-1 Vpu results in impaired migration and chemotactic signaling within CD4? T cells.
Academic Article Understanding the molecular manipulation of DCAF1 by the lentiviral accessory proteins Vpr and Vpx.
Academic Article HIV-1 Vpu utilizes both cullin-RING ligase (CRL) dependent and independent mechanisms to downmodulate host proteins.
Academic Article A Conserved HIV-1-Derived Peptide Presented by HLA-E Renders Infected T-cells Highly Susceptible to Attack by NKG2A/CD94-Bearing Natural Killer Cells.
Academic Article KIR3DL1 and HLA-B Density and Binding Calibrate NK Education and Response to HIV.
Academic Article HLA-C Downmodulation by HIV-1 Vpu.
Academic Article Inability of natural killer cells to destroy autologous HIV-infected T lymphocytes.
Academic Article Vectors derived from the human immunodeficiency virus, HIV-1.
Academic Article CD155 on HIV-Infected Cells Is Not Modulated by HIV-1 Vpu and Nef but Synergizes with NKG2D Ligands to Trigger NK Cell Lysis of Autologous Primary HIV-Infected Cells.
Academic Article HIV Latency-Reversing Agents Have Diverse Effects on Natural Killer Cell Function.
Academic Article Brief Report: Inflammatory Colonic Innate Lymphoid Cells Are Increased During Untreated HIV-1 Infection and Associated With Markers of Gut Dysbiosis and Mucosal Immune Activation.
Academic Article Plasma viral load, CD4+ cell counts, and HIV-1 production by cells.
Academic Article CD8+ cells from asymptomatic human immunodeficiency virus-infected individuals suppress superinfection of their peripheral blood mononuclear cells.
Academic Article Primary CD8+ cells from HIV-infected individuals can suppress productive infection of macrophages independent of beta-chemokines.
Academic Article Differences in HIV replication in CD4+ lymphocytes are not related to beta-chemokine production.
Academic Article The role of CD80 and CD86 in enhancing CD8(+) cell suppression of HIV replication.
Academic Article Effects of TH1 and TH2 cytokines on CD8+ cell response against human immunodeficiency virus: implications for long-term survival.
Academic Article Virological and immunological features of long-term human immunodeficiency virus-infected individuals who have remained asymptomatic compared with those who have progressed to acquired immunodeficiency syndrome.

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