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Full-Text Articles in Medicine and Health Sciences
Core-Binding Factor Influences The Disease Specificity Of Moloney Murine Leukemia Virus, Amy F. Lewis, Terryl Stacy, William R. Green, Lekidelu Taddesse-Heath, Janet W. Hartley, Nancy A. Speck
Core-Binding Factor Influences The Disease Specificity Of Moloney Murine Leukemia Virus, Amy F. Lewis, Terryl Stacy, William R. Green, Lekidelu Taddesse-Heath, Janet W. Hartley, Nancy A. Speck
Dartmouth Scholarship
The core site in the Moloney murine leukemia virus (Moloney MLV) enhancer was previously shown to be an important determinant of the T-cell disease specificity of the virus. Mutation of the core site resulted in a significant shift in disease specificity of the Moloney virus from T-cell leukemia to erythroleukemia. We and others have since determined that a protein that binds the core site, one of the core-binding factors (CBF) is highly expressed in thymus and is essential for hematopoiesis. Here we test the hypothesis that CBF plays a critical role in mediating pathogenesis of Moloney MLV in vivo. We …
Antiretroviral Cytolytic T-Lymphocyte Nonresponsiveness: Fasl/Fas-Mediated Inhibition Of Cd4+ And Cd8+ Antiviral T Cells By Viral Antigen-Positive Veto Cells, Robert F. Rich, William R. Green
Antiretroviral Cytolytic T-Lymphocyte Nonresponsiveness: Fasl/Fas-Mediated Inhibition Of Cd4+ And Cd8+ Antiviral T Cells By Viral Antigen-Positive Veto Cells, Robert F. Rich, William R. Green
Dartmouth Scholarship
C57BL/6 (H-2b ) mice generate type-specific cytolytic T-lymphocyte (CTL) responses to an immunodominant Kb-restricted epitope, KSPWFTTL located in the membrane-spanning domain of p15TM of AKR/Gross murine leukemia viruses (MuLV). AKR.H-2b congenic mice, although carrying the responder H-2b major histocompatibility complex (MHC) haplotype, are low responders or nonresponders for AKR/Gross MuLV-specific CTL, apparently due to the presence of inhibitory AKR.H-2b cells. Despite their expression of viral antigens and Kb, untreated viable AKR.H-2b spleen cells cause dramatic inhibition of the C57BL/6 (B6) antiviral CTL response to in vitro stimulation with AKR/Gross MuLV-induced …