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 3
Reversal of T cell inactivation during persistent viral infection. (A) SMARTA cells from LCMV Arm– (top panels) or Cl 13–infected (bottom panels) mice were isolated 10 days after infection and pooled separately. The numbers in each flow plot indicate the frequency of SMARTA cells on day 10 after LCMV Arm or Cl 13 infection that produced IFN-γ, TNF-α, and IL-2 prior to culture. SMARTA cells isolated on day 10 or 30 after Arm or Cl 13 virus infection were analyzed directly ex vivo or were sorted and cultured for 4 days. The bars in each graph indicate the percentage of IFN-γ–, TNF-α–, and IL-2–producing SMARTA cells prior to the ex vivo culture and following the 4-day culture. The individual bars indicate the frequency of SMARTA cells during LCMV Cl 13 infection that produce each cytokine represented as a percentage of SMARTA cells that produced the same cytokine during LCMV Arm infection. Each group contained cells pooled (prior to sorting) from 2–3 spleens, and the data are representative of at least 2 repeat experiments. (B) The ability of P14 cells (isolated from the same animals as represented in A) to produce IFN-γ, TNF-α, and IL-2 on day 10 after LCMV Arm or Cl 13 infection is shown in the dot plots, and the graphs illustrate the pre- (gray bars) and post-culture (black bars) levels of cytokine-producing P14 cells from LCMV Cl 13–infected animals represented as a percentage of the P14 response observed during LCMV Arm infection.