CTL-mediated protection against reinfection with LCMV and the onset of autoimmune diabetes in imatinib-treated mice. (A) Splenocytes (2.3 × 106) from LCMV immune C57BL/6 mice containing 5 × 104 gp33-specific memory CD8+ T cells were adoptively transferred into imatinib-treated (•; high-dose 50/100 regimen) and nontreated (▪) C57BL/6 recipients. The recipients had been infected intravenously with 104 pfu LCMV 10 hours earlier. Imatinib-treated and nontreated C57BL/6 mice infected intravenously at the same time point with 104 pfu LCMV, but not receiving memory CTLs, served as controls. LCMV titers in the spleens were measured 3 and 4 days after adoptive transfer, and the reduction of virus titer compared with controls was calculated. Results are given as the mean ± SEM of 3 to 4 mice per group. (B) Memory p14 splenocytes (8.2 × 106) containing 2 × 105 gp33-specific memory CD8+ T cells (Vα2+) were adoptively transferred into imatinib-treated (•; high-dose 50/100 regimen) and nontreated (▪) RIP-GP mice. One and 5 days later, RIP-GP mice were immunized intravenously with 2 × 105 H8-derived DCs, and blood-glucose concentration was measured at the time points indicated. Results are given as the mean ± SEM of 3 to 4 mice per group. Blood-glucose levels were statistically analyzed in imatinib-treated and nontreated mice 9 and 10 days after immunization. †Death of mice due to diabetes.
