Fig. 3.
Fig. 3. The donor CTL line was restricted through HLA-A11 and specific for EBNA-3B. / (A) The donor CTL line was tested for its ability to kill B95-8–derived LCLs from individuals who shared only one of each of its HLA class I antigens. Killing is shown across a range of effector:target ratios and was restricted mostly through HLA-A11. Killing through A2 and B60 was less than killing of an HLA class I MM-LCL. (B) The donor CTL line was EBNA-3B–specific. The donor, CR, shared HLA-A2, -A11, and -B7 with the CTL donor. This chromium release assay shows that the CR-LCLs and the donor LCLs were equally sensitive to killing by the donor CTL line. CR-derived dermal fibroblasts were infected with vaccinia virus recombinants expressing EBNAs 1, 2, 3A, 3B, 3C and LP as well as LMP1, LMP2, and the Escherichia coli–derived β-galactosidase gene. Only killing of EBNA-3B–expressing fibroblasts was greater than background killing of β-galactosidase–expressing fibroblasts.

The donor CTL line was restricted through HLA-A11 and specific for EBNA-3B.

(A) The donor CTL line was tested for its ability to kill B95-8–derived LCLs from individuals who shared only one of each of its HLA class I antigens. Killing is shown across a range of effector:target ratios and was restricted mostly through HLA-A11. Killing through A2 and B60 was less than killing of an HLA class I MM-LCL. (B) The donor CTL line was EBNA-3B–specific. The donor, CR, shared HLA-A2, -A11, and -B7 with the CTL donor. This chromium release assay shows that the CR-LCLs and the donor LCLs were equally sensitive to killing by the donor CTL line. CR-derived dermal fibroblasts were infected with vaccinia virus recombinants expressing EBNAs 1, 2, 3A, 3B, 3C and LP as well as LMP1, LMP2, and the Escherichia coli–derived β-galactosidase gene. Only killing of EBNA-3B–expressing fibroblasts was greater than background killing of β-galactosidase–expressing fibroblasts.

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