Naturally occurring leukemia viruses in H-2 congenic C57BL mice III. Characterization of C-type viruses isolated from lymphomas induced by milk transmission of B-ecotropic virus

Zijlstra, Maarten; Goede, R. E. Y. De; Schoenmakers, H. J.; Schinkel, Alfred H.; Hesselink, W.; Portis, John L.; Melief, Cornelis J.M.

doi:10.1016/0042-6822(83)90062-4

Cited by 20 publications

(18 citation statements)

References 35 publications

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“…Within one mouse strain, virus-induced T cell lymphomas arose earlier than B cell lymphomas after neonatal inoculation with a single cloned MuLV (Zijlstra et af., 1984). The H-2 complex has a marked influence on lymphoma type (Zijlstra et al, 1983(Zijlstra et al, , 1984 which confirms earlier observations made with an uncloned milk-transmitted ecotropic MuLV (Melief el af., 1980). The cloned oncogenic MCF 1233 also induced different types of lymphomas in H-2 congenic mice (Zijlstra et af., 1983(Zijlstra et af., , 1984, e.g.…”

Section: Introductionsupporting

confidence: 88%

THE H‐2 COMPLEX REGULATES BOTH THE SUSCEPTIBILITY TO MOUSE VIRAL LYMPHOMAGENESIS AND THE PHENOTYPE OF THE VIRUS‐INDUCED LYMPHOMAS

Zijlstra

Vasmel

Radaskiewicz³

et al. 1986

Int J Immunogenetics

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SUMMARY Neonatal infection of C57BL/10 mice with cloned ecotropic and/or dual‐tropic mink cell focus‐inducing (MCF) mouse leukaemia viruses (MuLV), induces a wide spectrum of different lymphomas of T, B, and non‐T/non‐B cell types. The H‐2 complex has a marked influence on both the development of lymphoma incidence and lymphoma type. A study using the oncogenic MCF 1233 virus and a series of B10 congenic mice enabled the mapping of the following: (a) Resistance to the early development of T cell lymphomas is controlled by the H‐21‐A locus. (b) Susceptibility to early T cell lymphomagenesis is associated with an I‐A‐regulated low anti‐MCF 1233 envelope antibody response and persistent infection of the thymus. (c) B10 (H‐2b) mice, which are resistant to early T cell lymphomagenesis induced by MCF 1233 or other MuLV isolates, have high anti‐MuLV envelope antibody responses which are I‐A‐regulated. These mice develop more B cell lymphomas late in life in contrast to the early development of T cell lymphoma in B10.A (H‐2a mice. The possible response mechanisms which underlie these observations, including: (1) I‐A ‐regulated immunoselection against MuLV antigens expressed by (pre) leukaemic T cells, (2) aberrant expression of class II MHC antigens on some B cell lymphomas and (3) I‐A‐regulated chronic immunostimulation of MuLV‐expressing (pre) leukaemic B cells, are discussed.

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Section: Introductionsupporting

confidence: 88%

THE H‐2 COMPLEX REGULATES BOTH THE SUSCEPTIBILITY TO MOUSE VIRAL LYMPHOMAGENESIS AND THE PHENOTYPE OF THE VIRUS‐INDUCED LYMPHOMAS

Zijlstra

Vasmel

Radaskiewicz³

et al. 1986

Int J Immunogenetics

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“…In marked contrast to T cell lymphomas, targeting of cellular oncogenes (Mucenski et al, 1987b) or involvement of MCF MuLVs has been reported only infrequently for B lineage tumors (Armstrong et al, 1980;Gilbert et al, 1993;Mucenski et al, 1987bMucenski et al, , 1988Pals et al, 1986;Thomas et al, 1990;Zijlstra et al, 1983Zijlstra et al, , 1986, but association of somatic ecotropic virus integrations in spontaneous pre-B or B cell lymphoma has been reported in certain AKXD RI strains (Gilbert et al, 1993;Justice et al, 1994;Mucenski et al, 1987a); CWD (Mucenski et al, 1988); SEA (Mucenski et al, 1988), C57BL , SL/Kh (Yamada et al, 1994), and in graft-versus-host reaction in CAF 1 mice (Pals et al, 1986). …”

Section: Discussionmentioning

confidence: 99%

“…It is noteworthy that studies using the Swiss mouse strain NMRI (Lovmand et al, 1998;Speth et al, 1995) uncovered a B lymphomagenic potential for Akv, the AKR-derived prototypic ecotropic MuLV strain, long considered nononcogenic, based on assays in other mouse strains. Other instances of B cell lymphoma induction by exogenous infection with either ecotropic or MCF MuLVs do not appear to be highly efficient (Thomas et al, 1990;Zijlstra et al, 1983;. B cell lymphomas, mostly pre B-LL, can be induced by retroviruses that contain oncogenes such as v-abl (Abelson and Rabstein, 1970), v-cbl (Langdon et al, 1989), v-myc (Morse et al, 1986), or constructs of v-myc and v-raf (Kurie et al, 1990) or by infection of E -myc transgenic mice with Moloney MuLV (Adams et al, 1985).…”

Section: Discussionmentioning

confidence: 99%

Accelerated Appearance of Multiple B Cell Lymphoma Types in NFS/N Mice Congenic for Ecotropic Murine Leukemia Viruses

Hartley

Chattopadhyay

Lander

et al. 2000

Laboratory Investigation

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SUMMARY:Spontaneous lymphomas occur at high frequency in NFS.V ϩ mice, strains congenic for ecotropic murine leukemia virus (MuLV) proviral genes and expressing virus at high titer. In the present study, a total of 703 NFS.V ϩ lymphomas were studied by histopathology, immunophenotypic analysis, immunoglobulin heavy chain or T cell receptor ␤ chain rearrangements, and somatic ecotropic MuLV integrations; 90% of the lymphomas tested were of B cell lineage. Low-grade tumors included small lymphocytic, follicular, and splenic marginal zone lymphomas, while high-grade tumors comprised diffuse large-cell (centroblastic and immunoblastic types), splenic marginal zone, and lymphoblastic lymphomas. Comparison of mice of similar genetic background except for presence (NFS.V ϩ ) or absence (NFS.V Ϫ ) of functional ecotropic MuLV genomes showed that NFS.V Ϫ clonal lymphomas developed at about one-half the rate of those occurring in NFS.V ϩ mice, and most were low-grade B cell lymphomas with extended latent periods. In NFS.V ϩ mice, clonal outgrowth, defined by Ig gene rearrangements, was associated with acquisition of somatic ecotropic proviral integrations, suggesting that, although generation of B cell clones can be virus independent, ecotropic virus may act to increase the rate of generation of clones and speed their evolution to lymphoma. The mechanism remains undefined, because only rare rearrangements were detected in several cellular loci previously associated with MuLV insertional mutagenesis. (Lab Invest 2000, 80:159-169).O ne of the earliest mammalian animal models in cancer research was the AKR mouse strain developed by Jacob Furth about 70 years ago. Selective breeding yielded mice with nearly 100% mortality due to thymic lymphoma in 7 to 14 months (Cole and Furth, 1941). AKR and the limited number of other T cell lymphoma-prone mouse strains (C58, HRS, and some AKXD recombinant inbred (RI) lines) (Gilbert et al, 1993;Green et al, 1980;MacDowell and Richter, 1935;Meier et al, 1969;Mucenski et al, 1986Mucenski et al, , 1988 have been intensively studied, yielding a partial molecular understanding of the role of ecotropic and recombinant mink cell focus-inducing (MCF) murine leukemia viruses (MuLV) in pathogenesis of this earlyonset lymphoma (Cloyd et al, 1980;Hartley et al, 1977;Holland et al, 1985; M c Grath and Weissman, 1979;Rowe and Hartley, 1983;Stoye et al, 1991;Thomas et al, 1984). In contrast to those of T cell lineage, spontaneous B cell lymphomas are most commonly seen in aged mice of strains in which T cell lymphoma does not predominate. For example, the incidence of B cell lymphoma of various types may be 30% or more in unmanipulated, aged BALB/c, C57BL (Frith and Wiley, 1981), AKR.Fv-1 b (HaranGhera et al, 1993), CWD (Angel and Bedigian, 1984;Mucenski et al, 1988;Thomas et al, 1989), or certain AKXD RI lines (Gilbert et al, 1993;Mucenski et al, 1986) held for up to 3 years, as well as in thymectomized AKR (Peled and Haran-Ghera, 1985) and Emyc transgenic mice (Adams et al, 1985). In SL/Kh (Shimada e...

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“…Primary lymphomas were induced by injection of newborn mice ofC57BL/10 or C57BL/6 background, carrying various H-2 haplotypes as listed in Table 1, with MCF 1233 MuLV as described (25). The origin and characteristics of MCF 1233 were described previously (26). This dualtropic B-tropic MuLV was biologically cloned from a T cell tumor, which arose in a B10.A mouse after milk transmission of a naturally occurring B-tropic ecotropic MuLV (27) .…”

Section: Methodsmentioning

confidence: 99%

Primary virus-induced lymphomas evade T cell immunity by failure to express viral antigens.

Vasmel

Sijts

Leupers

et al. 1989

The Journal of Experimental Medicine

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It is well established that MHC-restricted T cell responses decisively influence the outcome of virus infection (1-3). In the rejection of murine leukemia virus-induced lymphomas, Th and cytotoxic T (Tc) t cells are considered essential effector cells, besides the effects of MuLVspecific antibodies, which can neutralize the virus and inhibit its spread (reviewed in reference 4). Many attempts have been made to characterize the viral antigens that are important in recognition by murine leukemia virus (MuLV)-specific T cells. The presence of viral proteins on the cell surface of MuLV induced tumor cell lines has been documented in a number of serological studies. These cell surface viral proteins, which in processed form are potential target molecules for recognition by Th and Tc cells (5), include the viral env gene-encoded products gPr85env, gp70, and p15(E) and the gag gene-encoded gP95g°g, gP85g°g, p10, pp12, p30, and p15 (reviewed in reference 6). In addition to this, recent data indicate that viral proteins that are not detectable at the surface of cells by serology can also serve as targets for T cells (7). DNA-mediated gene transfer experiments, in which single MuW viral antigens together with particular MHC class I antigens were expressed in heterologous cell lines, and the availability of Tc clones have provided a more subtle analysis of MHC and viral antigen recognition (8, 9). A highly complex picture emerged from these studies, which collectively indicate that both MHC and non-MHC genes determine which viral antigens are recognized in the context of MHC.Recently, substantial progress has been made in the understanding of MHCrestricted recognition ofantigens by T cells. It now appears that T cells usually recognize relatively short antigenic peptides, derived by processing of the native antigen (10, 11). This holds for MHC class II-restricted antigen recognition at the surface of APC by Th cells, but also for MHC class I-restricted antigen recognition by Tc cells, which results in lysis of the antigenic peptide-bearing cells (7,12). The MHCpeptide interaction required for T cell recognition is rather MHC allele specific, which implies that the nature of viral antigens preferentially recognized differs from individual to individual (7,(13)(14)(15)(16)(17) .

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Naturally occurring leukemia viruses in H-2 congenic C57BL mice III. Characterization of C-type viruses isolated from lymphomas induced by milk transmission of B-ecotropic virus

Cited by 20 publications

References 35 publications

THE H‐2 COMPLEX REGULATES BOTH THE SUSCEPTIBILITY TO MOUSE VIRAL LYMPHOMAGENESIS AND THE PHENOTYPE OF THE VIRUS‐INDUCED LYMPHOMAS

THE H‐2 COMPLEX REGULATES BOTH THE SUSCEPTIBILITY TO MOUSE VIRAL LYMPHOMAGENESIS AND THE PHENOTYPE OF THE VIRUS‐INDUCED LYMPHOMAS

Accelerated Appearance of Multiple B Cell Lymphoma Types in NFS/N Mice Congenic for Ecotropic Murine Leukemia Viruses

Primary virus-induced lymphomas evade T cell immunity by failure to express viral antigens.

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