Header Logo

Search Result Details

Back to Search Results
This page shows the details of why an item matched the keywords from your search.
Search Results
Barker, Ed
One or more keywords matched the following properties of Barker, Ed
PropertyValue
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: https://www.rushu.rush.edu/faculty/edward-barker-phd My Laboratory: https://www.rushu.rush.edu/research/departmental-research/microbial-pathogens-and-immunity-research/laboratory-edward-barker-phd My NCBI Bibliography: https://www.ncbi.nlm.nih.gov/myncbi/browse/collection/46831905/?sort=date&direction=descending My Scopus: https://www.scopus.com/authid/detail.uri?authorId=7103411264 Education: PhD, University of Illinois
One or more keywords matched the following items that are connected to Barker, Ed
Item TypeName
Concept HIV Infections
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 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 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 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 Inability of natural killer cells to destroy autologous HIV-infected T lymphocytes.
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 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 Effects of TH1 and TH2 cytokines on CD8+ cell response against human immunodeficiency virus: implications for long-term survival.
Academic Article Contribution of Innate Lymphoid Cells in Supplementing Cytokines Produced by CD4+ T Cells During Acute and Chronic SIV Infection of the Colon.
Academic Article Differential effects of CD28 costimulation on HIV production by CD4+ cells.
Search Criteria
  • HIV Infections