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Showing papers on "Friend leukemia published in 1989"


Journal ArticleDOI
TL;DR: In a Friend retrovirus-induced tumor model in which tumor rejection can be mediated by either CTL or Th, antigens derived from discrete retroviral proteins are predominantly responsible for activation of each T cell subset.
Abstract: Immunization of C57BL/6 (B6) mice with FBL, a Friend murine leukemia virus (F-MuLV), induces both tumor-specific cytolytic CD8+ (CTL) and lymphokine-producing CD4+ Th that are effective in adoptive therapy of B6 mice bearing disseminated FBL leukemia. The current study evaluated the F-MuLV antigenic determinants expressed on FBL that are recognized by FBL-reactive CD8+ and CD4+ T cells. To identify the specificity of the FBL-reactive CD8+ CTL, Fisher rat embryo fibroblast (FRE) cells transfected with plasmids encoding F-MuLV gag or envelope (env) gene products plus the class I-restricting element Db were utilized. FBL-reactive CTL recognized FRE target cells transfected with the F-MuLV gag-encoded gene products, but failed to recognize targets expressing F-MuLV env. Attempts to generate env-specific CD8+ CTL by immunization with a recombinant vaccinia virus containing an inserted F-MuLV env gene were unsuccessful, despite the generation of a cytolytic response to vaccinia epitopes, implying that B6 mice fail to generate CD8+ CTL to env determinants. By contrast, CD4+ Th clones recognized FRE target cells transfected with env and not gag genes, and immunization with the recombinant vaccinia virus induced an env-specific CD4+ T cell response. These data show that in a Friend retrovirus-induced tumor model in which tumor rejection can be mediated by either CTL or Th, antigens derived from discrete retroviral proteins are predominantly responsible for activation of each T cell subset.

76 citations


Journal Article
01 Jan 1989-Leukemia
TL;DR: It is demonstrated that LAK cell plus rIL-2 treatment can induce permanent regressions in progressively leukemic mice and provide a responsive and manipulable model system to elucidate the mechanisms involved in this form of immunotherapy.
Abstract: The antileukemic effects of lymphokine-activated killer (LAK) cells plus recombinant interleukin-2 (rIL-2) therapy were assessed in mice with Friend virus (FV)-induced erythroleukemia. LAK cells were generated by incubating normal spleen cells for 72 hr in the presence of rIL-2 (1000 units/ml). At the time of injection, the LAK cells were cytotoxic in vitro against FV-infected fibroblasts and NK-sensitive and -resistant tumor targets but not normal controls. To determine in vivo activity, fully leukemic mice (spleen weight greater than 0.75 g) were injected with either PBS or LAK cells (10(8) cells/mouse IV at 14 and 17 days post virus) and rIL-2 (10,000 units/mouse IP every 8 hr on days 14 through 18 post virus). More than 70% of the progressively leukemic mice experienced permanent leukemia regressions (disease-free for greater than 100 days) following LAK cell plus rIL-2 therapy. Regressions were characterized by return of spleen and liver weights to normal and elimination of virus-infected erythroid (CFU-E) and macrophage (CFU-C) progenitor cells from spleen and marrow. Leukemic animals treated with either LAK cells alone or IL-2 alone experienced only transient leukemia regressions. These results demonstrate that LAK cell plus rIL-2 treatment can induce permanent regressions in progressively leukemic mice and provide a responsive and manipulable model system to elucidate the mechanisms involved in this form of immunotherapy.

19 citations


Journal ArticleDOI
TL;DR: It is expected that further investigation of the model will prove useful in several areas of AIDS research, including the development of efficacious drug therapies, and the understanding of the mechanisms whereby retroviruses immunosuppress their hosts.

16 citations


Journal ArticleDOI
TL;DR: Splenic proliferation of normal stem cells is apparently a host response to leukemogenesis, and it is proposed that it may contribute to certain retroviral diseases.
Abstract: Interleukin-3-dependent hematopoietic stem cells commonly accumulate in spleens of mice infected with leukemia viruses To study their origins, a molecularly tagged helper-free Friend spleen focus-forming virus was used to produce erythroleukemias Uninfected interleukin-3-dependent basophil-mast cell progenitors coproliferated amidst the spleen focus-forming virus-infected leukemic cells Splenic proliferation of normal stem cells is apparently a host response to leukemogenesis, and we propose that it may contribute to certain retroviral diseases

13 citations


Journal Article
TL;DR: These studies establish conditions whereby a small population of sensitive strain cells in an overwhelming background of resistant strain cells can be selectively expanded and could be useful in efforts to clone the Fv-2 gene.

8 citations


Journal ArticleDOI
TL;DR: Serial examination of five newly derived Friend murine tumors during early subcutaneous passages showed continuing changes in chromatin composition and structure over the first 10 to 20 passages followed by a period of stabilization over the subsequent 20 passages, suggesting that Friend tumor establishment is accompanied by an early period of Chromatin reorganization marked by changes in several parameters of chromatin structure.

8 citations


Journal ArticleDOI
TL;DR: Results obtained testing tumor growth in lethally irradiated hosts provide further support to the hypothesis that exogenous IFN capable of suppressing the growth of both lines could act via enhancement of the NR function.

6 citations


Journal ArticleDOI
TL;DR: Analysis of the spleens from mice infected with RB virus indicated that RB induced the early stage of Friend disease (erythroid proliferation) in both F v-2rr and Fv-2ss mice.

5 citations


Journal ArticleDOI
TL;DR: Results suggest that activation and expression of ecotropic and xenotropic endogenous sequences may play a role in pathogenesis of the disease.