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Table 1

Primary CTL Levels Found in RIP LCMV IFN-γ–deficient or –competent Mice

Effector day 7 splenocytesSpecific 51Cr release (%) from targets
H-2dH-2b
GroupE/TLCMVvv/GPNPpeplog pe*LCMVvv/GP
H-2d  50:1  78 ± 6   2 ± 1  39 ± 12  −9   
IFN-γ–competent  25:1  58 ± 9   36 ± 6     
H-2d  50:1  55 ± 12   2 ± 1  39 ± 8  −9   
IFN-γ–deficient  25:1  38 ± 11   29 ± 3     
RIP–NP, H-2d  50:1  28 ± 7  11 ± 4  20 ± 4  −7   
IFN-γ–competent  25:1  15 ± 4   3 ± 2  15 ± 3     
RIP–NP, H-2d  50:1  22 ± 7  12 ± 5  19 ± 3  −7   
IFN-γ–deficient  25:1   8 ± 4   4 ± 4  11 ± 4     
               
H-2b  50:1       55 ± 9  33 ± 7 
IFN-γ–competent  25:1       28 ± 6  16 ± 6 
H-2b  50:1       60 ± 9  32 ± 7 
IFN-γ–deficient  25:1       33 ± 5  20 ± 2 
RIP GP, H-2b  50:1       52 ± 4  36 ± 7 
IFN-γ–competent  25:1       22 ± 3  15 ± 5 
RIP GP, H-2b  50:1       60 ± 6  28 ± 8 
IFN-γ–deficient  25:1       38 ± 5  22 ± 8 
CTL assays were performed as described in the Materials and Methods section. Target cells were BALB/C17 (H-2d) fibroblasts uninfected or infected with LCMV (ARM), or vaccinia viruses expressing the complete LCMV GP (vv/GP). Background lysis of uninfected cells was <5% in all assays and was subtracted from the lysis (51Cr release) values shown. Five mice were tested per group and the mean +/− 1 SE is displayed. Primary CTL activity found in spleens was assessed on day 7 after LCMV infection. Affinities of antiself CTLs (*) were recorded according to the minimal concentration of LCMV-NP peptide (RPQASGVYM) required for lysis of target cells by CTLs. Note that high affinity CTLs found in non-tg mice require 2 logs less peptide for lysing target cells than low-affinity CTLs found in tg mice (27). Further, low affinity CTLs required 10 times less antiCD8 antibody to inhibit CTL killing by 50% (C50 [αCD8]) than high affinity CTLs from non-tg mice. 
Effector day 7 splenocytesSpecific 51Cr release (%) from targets
H-2dH-2b
GroupE/TLCMVvv/GPNPpeplog pe*LCMVvv/GP
H-2d  50:1  78 ± 6   2 ± 1  39 ± 12  −9   
IFN-γ–competent  25:1  58 ± 9   36 ± 6     
H-2d  50:1  55 ± 12   2 ± 1  39 ± 8  −9   
IFN-γ–deficient  25:1  38 ± 11   29 ± 3     
RIP–NP, H-2d  50:1  28 ± 7  11 ± 4  20 ± 4  −7   
IFN-γ–competent  25:1  15 ± 4   3 ± 2  15 ± 3     
RIP–NP, H-2d  50:1  22 ± 7  12 ± 5  19 ± 3  −7   
IFN-γ–deficient  25:1   8 ± 4   4 ± 4  11 ± 4     
               
H-2b  50:1       55 ± 9  33 ± 7 
IFN-γ–competent  25:1       28 ± 6  16 ± 6 
H-2b  50:1       60 ± 9  32 ± 7 
IFN-γ–deficient  25:1       33 ± 5  20 ± 2 
RIP GP, H-2b  50:1       52 ± 4  36 ± 7 
IFN-γ–competent  25:1       22 ± 3  15 ± 5 
RIP GP, H-2b  50:1       60 ± 6  28 ± 8 
IFN-γ–deficient  25:1       38 ± 5  22 ± 8 
CTL assays were performed as described in the Materials and Methods section. Target cells were BALB/C17 (H-2d) fibroblasts uninfected or infected with LCMV (ARM), or vaccinia viruses expressing the complete LCMV GP (vv/GP). Background lysis of uninfected cells was <5% in all assays and was subtracted from the lysis (51Cr release) values shown. Five mice were tested per group and the mean +/− 1 SE is displayed. Primary CTL activity found in spleens was assessed on day 7 after LCMV infection. Affinities of antiself CTLs (*) were recorded according to the minimal concentration of LCMV-NP peptide (RPQASGVYM) required for lysis of target cells by CTLs. Note that high affinity CTLs found in non-tg mice require 2 logs less peptide for lysing target cells than low-affinity CTLs found in tg mice (27). Further, low affinity CTLs required 10 times less antiCD8 antibody to inhibit CTL killing by 50% (C50 [αCD8]) than high affinity CTLs from non-tg mice. 
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