Document 0103 DOCN M9580103 TI Interleukin-12 augments the generation of autologous tumor-reactive CD8+ cytotoxic T lymphocytes from tumor-infiltrating lymphocytes. DT 9506 AU Kuge S; Watanabe K; Makino K; Tokuda Y; Mitomi T; Kawamura N; Habu S; Nishimura T; Department of Immunology, Tokai University School of Medicine,; Isehara. SO Jpn J Cancer Res. 1995 Feb;86(2):135-9. Unique Identifier : AIDSLINE MED/95247536 AB Human tumor-infiltrating lymphocytes (TIL) were obtained from breast cancer, renal cancer or neuroblastoma to investigate the generation of autologous tumor-reactive CD8+ cytotoxic T lymphocytes (CTL). When TIL were cultured with interleukin (IL)-2 (100 U/ml), the growth of TIL peaked around 8-10 days after the initiation of culture. In contrast, the proliferation of TIL cultured with IL-2 plus IL-12 peaked around 4-5 days after culture and tumor cells rapidly disappeared from the culture. To determine the generation of autologous tumor-reactive CD8+ CTL, TIL-derived CD8+ T cells were separated by FACStar. Both IL-2-activated and IL-2 plus IL-12-activated TIL-CD8+ T cells showed the same level of lymphokine-activated killer activity against a variety of tumor cells. However, TIL-CD8+ T cells activated with IL-2 plus IL-12 revealed greatly augmented cytotoxicity against autologous tumor cells compared with that induced by IL-2 alone. The autologous tumor cell-killing activity of TIL-CD8+ CTL was significantly inhibited by the addition of F(ab)2 anti-CD3 monoclonal antibody, indicating that these CTL recognize autologous tumor antigen through T cell receptor. These results imply that IL-12 is a novel cytokine which facilitates the generation of autologous tumor-reactive CD8+ CTL from TIL. DE CD8-Positive T-Lymphocytes/*DRUG EFFECTS Human Interleukin-12/*PHARMACOLOGY Interleukin-2/PHARMACOLOGY Lymphocytes, Tumor-Infiltrating/*DRUG EFFECTS Support, Non-U.S. Gov't Tumor Cells, Cultured JOURNAL ARTICLE SOURCE: National Library of Medicine. NOTICE: This material may be protected by Copyright Law (Title 17, U.S.Code).