MHC and B7-1 promoted rejection of allogeneic tumors in RAG-1(-/-) mice. (A) Phenotypes of tumor cells used in this study. Tumor cells were stained with 28-14-8 (BD Pharmingen), a mAb specific for H-2L^d (upper panel) or 3A12, a mAb for B7-1 (lower panel).⁵⁹  Solid thin lines: J558 cells were transfected with vector alone (hereby called MHC⁺B7^-). Dashed lines: J558 cells transfected with B7-1 (MHC⁺B7⁺). Bold lines: an MHC loss variant of the MHC⁺B7⁺ tumor cell line (MHC^-B7⁺). (B) B7-dependent rejection of tumor cells by NK cells. RAG-1(-/-) mice were treated with either PBS or the Tmβ1 mAb prior to tumor challenge. The incidences (upper panel) and tumor sizes (lower panel) were determined by physical examination. Data shown are a summary of 3 (no depletion) or 2 (NK depleted) independent experiments with a total of 7 (NK depleted) or 10 (PBS treated) mice per group. (C) B7-1 enhanced rejection of MHC class I⁺, but not MHC class I^-, tumor cells by NK cells. RAG-1(-/-) mice were challenged with MHC⁺B7^-, MHC⁺B7⁺, MHC^-B7⁺ (n = 5). Data shown in panel C are representative of 2 independent experiments.