Reprogramming of antiviral T cells prevents inactivation and restores T cell activity during persistent viral infection
J. Clin. Invest. David G. Brooks, et al. 116:1675 doi:10.1172/JCI26856 [Go to this article.]

Figure 2
T cell function is not programmed during priming but is an ongoing process. (A) SMARTA and P14 cells were cotransferred into mice, followed 2 days later by infection with LCMV Arm or Cl 13. Five days after infection, following T cell priming, splenocytes from LCMV Arm– or Cl 13–infected mice were isolated and pooled separately. B cells were depleted by positive selection, and the remaining “untouched” splenocytes were transferred into recipient mice infected in parallel with LCMV Arm or Cl 13 five days earlier but not given SMARTA and P14 cells. T cells from the recipient mice were analyzed at 9 and 40 days after infection. (B and C) Cotransferred SMARTA and P14 cells were primed in LCMV Arm– or Cl 13–infected animals for 5 days and then transferred into mice infected in parallel with either LCMV Arm or Cl 13 four (top panels) and 35 (bottom panels) days following transfer of the primed cells (days 9 and 40 after infection, respectively). Splenocytes from each mouse were isolated, and the ability of the cotransferred SMARTA (B) and P14 cells (C) to produce IFN-γ, TNF-α, and IL-2 was analyzed by intracellular flow cytometry. The type of infection in which the cells were primed is indicated underneath each graph. Gray and black bars represent transfer into LCMV Arm– and Cl 13–infected recipients, respectively. The bars represent the average ± SD of 4 mice in each group and are representative of 2–4 experiments. Note that the scales on the y axis differ for the cytokines analyzed. *Statistically significant difference (P ≤ 0.05) between cells primed in the same environment and then transferred into LCMV Arm– or Cl 13–infected animals; **P ≤ 0.01.