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 1
Virus-specific CD4⁺ and CD8⁺ T cells lose initially strong activity during the establishment of a persistent viral infection. (A) Spleens were isolated from LCMV Arm– (open diamonds) and Cl 13–infected (filled squares) animals and titers of infectious virus determined by plaque assay. Data are expressed as plaque forming units per gram of spleen. The dashed line indicates the lower limit of detection (200 PFU/g spleen). Each time point represents the average ± 1 SD of 3 mice per group. (B and C) LCMV-specific SMARTA (TCR Tg CD4⁺ T cells) (B) and P14 (TCR Tg CD8⁺ T cells) cells (C) were cotransferred into mice that were subsequently infected with LCMV Arm or Cl 13. On days 5 (left panels) and 9 (right panels) after infection, splenocytes from individual mice were isolated and the frequency of IFN-γ–, TNF-α–, and IL-2–producing SMARTA and P14 cells assessed by intracellular cytokine staining. The flow plots are gated on SMARTA (B) and P14 (C) cells, and the values represent the percentage of cytokine-producing cells. The flow plots are representative of 4 independent experiments containing 4 mice per group.