The tumor lines are less sensitive to killing by HLA class I–restricted CTLs, even though they have no defect in antigen presentation.

(A) The tumor lines are less sensitive to killing than the donor LCLs. To compare the sensitivity of donor-derived B95-8 virus–transformed B-cell line and the recipient-derived tumor cell lines to killing by the donor CTL line, donor CTLs were incubated with⁵¹Cr-labeled target cells for 4 hours in a standard chromium release assay at the effector:target ratios indicated. The target cells were the B95-8 virus–transformed donor LCLs, the patient-derived tumor lines that grew spontaneously from patient blood before and 7 days after CTL infusion, an HLA mismatched LCL (MM-LCL), and the LAK cell–sensitive target, HSB-2. (B) Antitumor activity was HLA-restricted. To determine whether the antitumor activity of the CTL line was due to CTL or LAK cell activity, target cells were incubated with standard blocking antibodies to HLA class I (W6/32) and class II (CR3/43). After 30 minutes of incubation, effector cells were added at an effector:target ratio of 10:1. After 4 hours, the plates were harvested and the percent chromium release calculated. Killing of both tumor lines was HLA class I–restricted. (C) The tumor line is killed through HLA-B7. CHJ is HLA-matched at HLA loci A2, B7 with the donor. In a standard cytotoxicity assay, CHJ CTLs kill the pre-CTL tumor line with similar efficiency as they kill normal LCLs that share only A2 and B7. The killing is likely specific for B7 because LCLs that only match at A2 are not killed. (D) The tumor line is killed through HLA-B60. RF is HLA-matched at HLA loci A2, B60 with the donor. In a standard cytotoxicity assay, RF-CTLs kill the pre-CTL tumor line with similar efficiency as they kill normal LCLs that share A2 and B60. The killing is likely specific for B60 because LCLs who only match A2 are not killed.