CD8 T cell defect of TNF-α and IL-2 in DNAM-1 deficient mice delays clearance in vivo of a persistent virus infection
Copyright policy )CD8 T cell defect of TNF-α and IL-2 in DNAM-1 deficient mice delays clearance in vivo of a persistent virus infection
DNAM-1 gene-deficient (-/-) mice take significantly longer to clear an acute and persistent LCMV infection in vivo than DNAM-1 +/+ mice. During acute LCMV priming, at the single cell level, DNAM-1 -/- mice made significantly less cytoplasmic CD8 TNF-α and IL-2 but not IFN-γ than their DNAM-1 +/+ counterparts. Restimulated immune memory CD8 T cells from DNAM-1 -/- and DNAM-1 +/+ mice were equivalent in cytolytic activity against LCMV-infected target cells but DNAM-1 -/- CD8 T cells had significant reductions in TNF-α and IL-2 that were associated on adoptive transfer with the inability to terminate the persistent viral infection.
- Washington University in St. Louis School of Medicine United States
- Department of Pathology and Immunology Washington University School of Medicine United States
- Washington University in St. Louis United States
- Washington University in St. Louis United States
- University of Mary United States
Antigens, Differentiation, T-Lymphocyte, Male, Mice, Knockout, DNAM-1 deficiency, Acute LCMV infection, T Lineage-Specific Activation Antigen 1, Tumor Necrosis Factor-alpha, T cell defects, Persistent LCMV infection, CD8-Positive T-Lymphocytes, Adoptive Transfer, Mice, Inbred C57BL, Disease Models, Animal, Mice, Virology, Animals, Arenaviridae Infections, Interleukin-2, Lymphocytic choriomeningitis virus
Antigens, Differentiation, T-Lymphocyte, Male, Mice, Knockout, DNAM-1 deficiency, Acute LCMV infection, T Lineage-Specific Activation Antigen 1, Tumor Necrosis Factor-alpha, T cell defects, Persistent LCMV infection, CD8-Positive T-Lymphocytes, Adoptive Transfer, Mice, Inbred C57BL, Disease Models, Animal, Mice, Virology, Animals, Arenaviridae Infections, Interleukin-2, Lymphocytic choriomeningitis virus
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