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Program in Immunology and Virology, and
Department of Pathology, University of Massachusetts Medical Center, Worcester, MA 01655
Infection 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-
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.
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