scholarly journals FBL-reactive CD8+ cytotoxic and CD4+ helper T lymphocytes recognize distinct Friend murine leukemia virus-encoded antigens.

1989 ◽  
Vol 169 (2) ◽  
pp. 457-467 ◽  
Author(s):  
J P Klarnet ◽  
D E Kern ◽  
K Okuno ◽  
C Holt ◽  
F Lilly ◽  
...  
Keyword(s):  
T Cell ◽  
Vaccinia Virus ◽  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Recombinant Vaccinia Virus ◽  
Tumor Rejection ◽  
Target Cells ◽  
Gene Products ◽  
Recombinant Vaccinia ◽  
Murine Leukemia

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.

Tumor progression in murine leukemia virus-induced T-cell lymphomas: monitoring clonal selections with viral and cellular probes.

1986 ◽  
Vol 60 (1) ◽  
pp. 230-241 ◽  
Author(s):  
H T Cuypers ◽  
G C Selten ◽  
M Zijlstra ◽  
R E de Goede ◽  
C J Melief ◽  
...  
Keyword(s):  
T Cell ◽  
Tumor Progression ◽  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
T Cell Lymphomas ◽  
Cellular Probes ◽  
Murine Leukemia

scholarly journals Specificity studies on cytolytic T lymphocytes directed against murine leukemia virus-induced tumors. Analysis of monoclonal cytolytic T lymphocytes.

1982 ◽  
Vol 155 (4) ◽  
pp. 1050-1062 ◽  
Author(s):  
F Plata
Keyword(s):  
T Lymphocytes ◽  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Target Cells ◽  
Cytolytic T Lymphocytes ◽  
Tumor Target ◽  
Induced Tumors ◽  
Definition Of ◽  
Leukemia Viruses ◽  
Murine Leukemia

The specificities of cloned cytolytic T lymphocytes (CTL) were studied for the analysis of CTL populations generated against murine leukemia viruses (MuLV) in H-2 congenic BALB/c (H-2d) and BALB.B (H-2b) mice. In particular, CTL generated in response to tumors induced by Gross MuLV and Friend MuLV were studied; these tumors expressed virus-induced antigens that do not cross-react and that can be distinguished from each other. The systematic study of 92 CTL clones clearly indicated that MuLV-immune CTL were highly heterogeneous with respect to both the intensities of target cell lysis that they mediated and to their specificity of recognition of MuLV-induced tumor target cells. Various categories of CTL clones were identified, ranging from CTL clones tht were tightly H-2 restricted and specific for the immunizing tumor to CTL clones that displayed no discernible patterns of specificity and that attacked a large number of different target cells. In addition, the surface markers of these cloned CTL were defined, and the best conditions for their prolonged maintenance in culture were determined. The present data indicate that future efforts in the definition of target antigens recognized by tumor-specific CTL should be performed with monoclonal lymphocytes.

scholarly journals Mutation of All Runx (AML1/Core) Sites in the Enhancer of T-Lymphomagenic SL3-3 Murine Leukemia Virus Unmasks a Significant Potential for Myeloid Leukemia Induction and Favors Enhancer Evolution toward Induction of Other Disease Patterns

2004 ◽  
Vol 78 (23) ◽  
pp. 13216-13231 ◽  
Author(s):  
Karina Dalsgaard Sørensen ◽  
Leticia Quintanilla-Martinez ◽  
Sandra Kunder ◽  
Jörg Schmidt ◽  
Finn Skou Pedersen
Keyword(s):  
T Cell ◽  
Murine Leukemia Virus ◽  
Myeloid Leukemia ◽  
Leukemia Virus ◽  
Color Flow ◽  
Potent Inducer ◽  
Induced Tumors ◽  
Myeloid Leukemias ◽  
T Lymphomas ◽  
Murine Leukemia

ABSTRACT SL3-3 murine leukemia virus is a potent inducer of T-lymphomas in mice. Using inbred NMRI mice, it was previously reported that a mutant of SL3-3 with all enhancer Runx (AML1/core) sites disrupted by 3-bp mutations (SL3-3dm) induces predominantly non-T-cell tumors with severely extended latency (S. Ethelberg, J. Lovmand, J. Schmidt, A. Luz, and F. S. Pedersen, J. Virol. 71:7273-7280, 1997). By use of three-color flow cytometry and molecular and histopathological analyses, we have now performed a detailed phenotypic characterization of SL3-3- and SL3-3dm-induced tumors in this mouse strain. All wild-type induced tumors had clonal T-cell receptor β rearrangements, and the vast majority were CD3+ CD4+ CD8− T-lymphomas. Such a consistent phenotypic pattern is unusual for murine leukemia virus-induced T-lymphomas. The mutant virus induced malignancies of four distinct hematopoietic lineages: myeloid, T lymphoid, B lymphoid, and erythroid. The most common disease was myeloid leukemia with maturation. Thus, mutation of all Runx motifs in the enhancer of SL3-3 severely impedes viral T-lymphomagenicity and thereby discloses a considerable and formerly unappreciated potential of this virus for myeloid leukemia induction. Proviral enhancers with complex structural alterations (deletions, insertions, and/or duplications) were found in most SL3-3dm-induced T-lymphoid tumors and immature myeloid leukemias but not in any cases of myeloid leukemia with maturation, mature B-lymphoma, or erythroleukemia. Altogether, our results indicate that the SL3-3dm enhancer in itself promotes induction of myeloid leukemia with maturation but that structural changes may arise in vivo and redirect viral disease specificity to induction of T-lymphoid or immature myeloid leukemias, which typically develop with moderately shorter latencies.

scholarly journals G100R Mutation within 4070A Murine Leukemia Virus Env Increases Virus Receptor Binding, Kinetics of Entry, and Viral Transduction Efficiency

2003 ◽  
Vol 77 (1) ◽  
pp. 739-743 ◽  
Author(s):  
Chi-Wei Lu ◽  
Lucille O'Reilly ◽  
Monica J. Roth
Keyword(s):  
Viral Entry ◽  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Cell Types ◽  
Transduction Efficiency ◽  
Target Cells ◽  
Multiple Cell ◽  
Viral Transduction ◽  
Kinetics Of ◽  
Murine Leukemia

ABSTRACT Passage of 4070A murine leukemia virus (MuLV) in D17 cells resulted in a G-to-R change at position 100 within the VRA of the envelope protein (Env). Compared with 4070A MuLV, virus with the G100R Env displayed enhanced binding on target cells, internalized the virus more rapidly, and increased the overall viral titer in multiple cell types. This provides a direct correlation between binding strength and efficiency of viral entry. Deletion of a His residue at the SU N terminus eliminated the transduction efficiency by the G100R virus, suggesting that the G100R virus maintains the regulatory characteristics of 4070A viral entry. The improved transduction efficiency of G100R Env would be an asset for gene delivery systems.

scholarly journals Identification of a new common provirus integration site in gross passage A murine leukemia virus-induced mouse thymoma DNA.

1987 ◽  
Vol 7 (1) ◽  
pp. 512-522 ◽  
Author(s):  
R Villemur ◽  
Y Monczak ◽  
E Rassart ◽  
C Kozak ◽  
P Jolicoeur
Keyword(s):  
T Cell ◽  
Murine Leukemia Virus ◽  
Cell Transformation ◽  
Integration Site ◽  
Leukemia Virus ◽  
Tumor Development ◽  
Mouse Strains ◽  
Mouse Tumor ◽  
Provirus Integration ◽  
Murine Leukemia

The Gross passage A murine leukemia virus (MuLV) induced T-cell leukemia of clonal (or oligoclonal) origin in inoculated mice. To study the role of the integrated proviruses in these tumor cells, we cloned several newly integrated proviruses (with their flanking cellular sequences) from a single tumor in procaryotic vectors. With each of the five clones obtained, a probe was prepared from the cellular sequences flanking the provirus. With one such probe (SS8), we screened several Gross passage A MuLV-induced SIM.S mouse tumor DNAs and found that, in 11 of 40 tumors, a provirus was integrated into a common region designated Gin-1. A 26-kilobase-pair sequence of Gin-1 was cloned from two lambda libraries, and a restriction map was derived. All proviruses were integrated as a cluster in the same orientation within a 5-kilobase-pair region of Gin-1, and most of them had a recombinant structure of the mink cell focus-forming virus type. The frequency of Gin-1 occupancy by provirus was much lower in thymoma induced by other strains of MuLV in other mouse strains. Using somatic-cell hybrid DNAs, we mapped Gin-1 on mouse chromosome 19. Gin-1 was not homologous to 16 known oncogenes and was distinct from the other common regions for provirus integration previously described. Therefore, Gin-1 appears to represent a new common provirus integration region. The integration of a provirus within Gin-1 might be an important event leading to T-cell transformation, and the Gin-1 region might harbor sequences which are involved in tumor development.

Cell-free synthesis of a precursor polyprotein containing both gag and pol gene products by Rauscher murine leukemia virus 35S RNA

Cell ◽  
1978 ◽  
Vol 13 (2) ◽  
pp. 359-369 ◽  
Author(s):  
Edwin C. Murphy ◽  
John J. Kopchick ◽  
Kenneth F. Watson ◽  
Ralph B. Arlinghaus
Keyword(s):  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Gene Products ◽  
Murine Leukemia
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