TABLE 1.
Transgenic H-2b mice expressing LCMV NP in their thymus generate smaller numbers of LCMV NP CTL than do their nontransgenic littermatesa
| Type of mouse | LCMV pCTL countsb on cells coated with:
|
|
|---|---|---|
| GP-1 pept | NP-pept | |
| p+/+ (H-2b) | 1/180, 1/55, 1/320, 1/150 | 1/300, 1/125, 1/88, 1/450 |
| p+/− NP− | 1/230, 1/98, 1/255, 1/225 | 1/250, 1/78, 1/126, 1/380 |
| p+/− NP+ | 1/420, 1/133, 1/550, 1/480 | 1/4,550, 1/3,670, 1/5,670, 1/8,500 |
| p−/− NP− | NDc | ND |
| p−/− NP+ | ND | ND |
Groups of four RIP-NP thymic expressors and nontransgenic littermates were infected with 105 PFU of LCMV intraperitoneally. At 7 days postinfection, single-cell suspensions were prepared from spleens and tested for numbers of pCTL by limiting-dilution analysis (see Materials and Methods). The cutoff for positive wells for each responder cell concentration was killing of >3 standard errors over background 51Cr release. CTL activity was assessed by a 51Cr release assay in vitro, using syngeneic MC57 (H-2b) and MHC mismatched BalbCL/7 (H-2d) fibroblasts as targets. LCMV NP peptide (FQPQNGQFI) or GP-1 peptide was added to target cells in order to assess CTL specificity. The standard error for controls was <10%, and nonspecific 51Cr release was <5%. All control samples were run in triplicates with standard error of <5%; specific control killing of B6 spleens (day 7 postinfection) was 65% on NP peptide (NP-pept)-coated MC57 cells and 41% on GP-1 (GP-1 pept)-coated MC57 cells.
Results are given individually for the four mice in each group.
ND, not detected.