Abstract
In mice acutely infected with a moderate dose of lymphocytic choriomeningitis virus (LCMV), the frequencies of CD8 T cells detected by MHC tetramers and MHC dimers correlate well with the total number of activated CD8 T cells and with the frequencies of antigen-specific cells detected by peptide-induced intracellular IFN-γ assays (2)(3)(4); these same effector cells are highly cytotoxic against targets pulsed with LCMV-encoded peptides. The frequencies of T cells that seed the memory pool are functions of the clonal burst size of T cells during the acute response (5); this burst size is very high in the LCMV system, and, as a consequence, 10–15% of the spleen CD8 T cells remain specific for LCMV in the memory pool (2)(4). In this memory state, there remains excellent concordance among the MHC tetramer, MHC dimer, and intracellular IFN-γ assays (2)(4). The memory pool specific for each of these LCMV epitopes remains functional and stable in the absence of immune system perturbance, but other infections can disrupt this memory pool by displacing the LCMV-specific T cells with memory T cells of other specificities (4).