PMID- 6194224 OWN - NLM STAT- MEDLINE DCOM- 19831123 LR - 20071115 IS - 0022-1767 (Print) IS - 0022-1767 (Linking) VI - 131 IP - 4 DP - 1983 Oct TI - Characterization of alloimmunization-induced T lymphocytes reactive against AKR leukemia in vitro and correlation with graft-vs-leukemia activity in vivo. PG - 2050-8 AB - We have reported that immunization of H-2k mice with lymphoid cells from various allogeneic strains induced a population of cells that could eliminate first-passage spontaneous AKR leukemia from the spleens of immuno-suppressed AKR (H-2k) hosts. In the present study, we examined the nature of the cells responsible for this graft-vs-leukemia (GVL) reaction and compared them to cytolytic cells detected in vitro. Spleen cells from alloimmunized CBA/J (H-2k) mice were selectively depleted of various subpopulations by treatment with antibody and complement (C), then tested in vivo for GVL reactivity. Cell suspensions depleted of Thy-1.2+, Lyt-1+, or Lyt-2+ lymphocytes had no significant GVL reactivity, whereas suspensions depleted of NK-1.2+ cells retained GVL reactivity. The GVL-reactive cells persisted in H-2-compatible donor mice for up to 56 days. Lyt-1+2+ lymphocytes that were cytotoxic for cultured AKR leukemia cells in vitro could be detected in the spleens of alloimmunized H-2-compatible mice after expansion of the cells in T cell growth factor. Using quantitative limiting dilution cytotoxicity assays, we found that the frequency of leukemia-reactive cytotoxic lymphocytes (CL) in the spleen showed a direct correlation with the GVL efficacy of the cells in vivo. Alloimmunization was essential for induction of the GVL-reactive cell population. CL in alloimmunized mice consisted of heterogeneous cytotoxic specificities; i.e., some CL were leukemia-specific, others lysed only nonleukemic AKR target cells, and a third group mediated killing of both leukemic and nonleukemic target cells. The CL appeared to be H-2 restricted and specific for non-H-2 antigens shared by the AKR leukemia and the alloimmunizing cells. FAU - Truitt, R L AU - Truitt RL FAU - Shih, C Y AU - Shih CY FAU - Lefever, A V AU - Lefever AV FAU - Tempelis, L D AU - Tempelis LD FAU - Andreani, M AU - Andreani M FAU - Bortin, M M AU - Bortin MM LA - eng GR - CA 20484/CA/NCI NIH HHS/United States GR - CA 26245/CA/NCI NIH HHS/United States PT - Journal Article PT - Research Support, Non-U.S. Gov't PT - Research Support, U.S. Gov't, P.H.S. PL - United States TA - J Immunol JT - Journal of immunology (Baltimore, Md. : 1950) JID - 2985117R RN - 0 (Epitopes) RN - 0 (H-2 Antigens) SB - IM MH - Animals MH - Cytotoxicity, Immunologic MH - Dose-Response Relationship, Immunologic MH - Epitopes/analysis MH - *Graft vs Host Reaction MH - H-2 Antigens/administration & dosage MH - Immunologic Memory MH - Leukemia, Experimental/*immunology MH - Leukemia, Lymphoid/*immunology MH - Lymphocyte Depletion MH - Lymphocyte Transfusion MH - Lymphocytes/immunology MH - Mice MH - Mice, Inbred AKR MH - Mice, Inbred C57BL MH - Mice, Inbred CBA MH - Mice, Inbred DBA MH - T-Lymphocytes/classification/*immunology MH - T-Lymphocytes, Cytotoxic/immunology/transplantation EDAT- 1983/10/01 00:00 MHDA- 1983/10/01 00:01 CRDT- 1983/10/01 00:00 PHST- 1983/10/01 00:00 [pubmed] PHST- 1983/10/01 00:01 [medline] PHST- 1983/10/01 00:00 [entrez] PST - ppublish SO - J Immunol. 1983 Oct;131(4):2050-8.