Independent regulation of lymphocytic choriomeningitis virus-specific T cell memory pools: relative stability of CD4 memory under conditions of CD8 memory T cell loss
UMass Chan AffiliationsDepartment of Pathology
Program in Immunology and Virology
Graduate School of Biomedical Sciences
KeywordsAcute Disease; Amino Acid Sequence; Animals; Antigens; CD4-Positive T-Lymphocytes; CD8-Positive T-Lymphocytes; Cell Death; Epitopes, T-Lymphocyte; Hemocyanin; Hemorrhagic Fever, American; Herpesviridae Infections; *Immunologic Memory; Immunophenotyping; Injections, Intraperitoneal; Interferon Type II; Intracellular Fluid; Lymphocyte Activation; Lymphocyte Count; Lymphocytic Choriomeningitis; Lymphocytic choriomeningitis virus; Male; Mice; Mice, Inbred BALB C; Mice, Inbred C57BL; Molecular Sequence Data; Staining and Labeling; Stem Cells; T-Lymphocyte Subsets; Vaccinia
Medicine and Health Sciences
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AbstractInfection of mice with a series of heterologous viruses causes a reduction of memory CD8(+) T cells specific to viruses from earlier infections, but the fate of the virus-specific memory CD4(+) T cell pool following multiple virus infections has been unknown. We have previously reported that the virus-specific CD4(+) Th precursor (Thp) frequency remains stable into long-term immunity following lymphocytic choriomeningitis virus (LCMV) infection. In this study, we questioned whether heterologous virus infections or injection with soluble protein CD4 Ags would impact this stable LCMV-specific CD4(+) Thp memory pool. Limiting dilution analyses for IL-2-producing cells and intracellular cytokine staining for IFN-gamma revealed that the LCMV-specific CD4(+) Thp frequency remains relatively stable following multiple heterologous virus infections or protein Ag immunizations, even under conditions that dramatically reduce the LCMV-specific CD8(+) CTL precursor frequency. These data indicate that the CD4(+) and CD8(+) memory T cell pools are regulated independently and that the loss in CD8(+) T cell memory following heterologous virus infections is not a consequence of a parallel loss in the memory CD4(+) T cell population.
J Immunol. 2001 Feb 1;166(3):1554-61.
Permanent Link to this Itemhttp://hdl.handle.net/20.500.14038/32743
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