Differences in oncogenicity among murine leukemia virus isolates are not correlated with the magnitude of H-2 regulated anti-viral envelope antibody responses

Zijlstra, Maarten; Schoenmakers, H. J.; Melief, Cornelis J.M.

doi:10.1016/0145-2126(86)90057-3

Cited by 3 publications

(2 citation statements)

References 37 publications

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“…Several studies indicate that antiviral antibodies protect, albeit partially, against replication of MuLV in vivo (21,50,56). In previous studies, we have shown that both titer and subclass of antiviral antibodies produced following various modes of infection with ecotropic MuLV and MCF viruses including MCF 1233 are under H-2-linked regulation (53,54,58,62). The antibody response to MuLV is primarily directed at the envelope proteins gp7O and pl5E (21).…”

Section: Discussionmentioning

confidence: 98%

Major histocompatibility complex class II-regulated immunity to murine leukemia virus protects against early T- but not late B-cell lymphomas

Vasmel

Zijlstra

Radaszkiewicz

et al. 1988

J Virol

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We studied the relative importance of class I and class II major histocompatibility complex (MHC) immunoregulation in the control of Tand B-cell lymphomas induced by murine leukemia virus. Previously, we have described a mink cell focus-inducing (MCF) murine leukemia virus, MCF 1233, which induces not only lymphoblastic T-cell lymphomas but also follicle center cell or lymphoblastic B-cell lymphomas. We now report that the outcome of neonatal infection with MCF 1233 in H-2-congenic C57BL/10 and C57BL/6 mice is decisively influenced by the H-2 I-A locus. A total of 64% of H-2 I-Ak, d mice [B1O.BR, B10.D2, B10.A(2R), B10.A(4R), and B10.MBR] developed T-cell lymphomas after MCF 1233 infection (mean latency, 37 weeks). In contrast, H-2 I-Ab [B10, B10.A(5R), B6], H-2 I_Ab/k [(B10.A x B10)F1 and (BlO x B10.A)F1], and H-2 * Corresponding author.

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Section: Discussionmentioning

confidence: 98%

Major histocompatibility complex class II-regulated immunity to murine leukemia virus protects against early T- but not late B-cell lymphomas

Vasmel

Zijlstra

Radaszkiewicz

et al. 1988

J Virol

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“…How retroviruses adapt to the environment encountered in a newly infected host has not been well studied. Immune responses to retroviral envelope proteins are regulated by MHC genes (45)(46)(47). Passage of the Gross MuLV in BALB/c-H-2k mice results in the generation of variant viruses that have lost specific gp70en°epitopes (48) .…”

Section: Resultsmentioning

confidence: 99%

A host gene regulates the structure of the transmembrane envelope protein of murine leukemia viruses.

Coppola

Thomas

1990

The Journal of Experimental Medicine

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Heterogeneity in the structure of the envelope proteins has been observed in many human and animal retroviruses and may influence pathogenicity. However, the biological significance of this heterogeneity and the mechanisms by which it is generated are poorly understood. We have studied a mouse model in which the envelope gene structure of lymphoma-associated viruses appears to be controlled by a single host gene. The inoculation of HRS and CWD mice with a leukemogenic murine leukemia virus (MuLV) results in recombination between the injected virus and envelope gene sequences of endogenous retroviruses. The genomes of HRS (class I) env recombinants and CWD (class II) env recombinants differ in the sequences encoding the NH2-terminal portion of the transmembrane envelope protein (TM). We have shown that an HRS gene linked to the MHC on chromosome 17 mediates a dominant selection for recombinant retroviruses with the class I envelope gene structure. CBA mice, which share the H-2k haplotype with HRS, also carry the dominant allele at this locus. This system provides a useful model for studies of host factors involved in the selection of specific variants of pathogenic retroviruses.

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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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Differences in oncogenicity among murine leukemia virus isolates are not correlated with the magnitude of H-2 regulated anti-viral envelope antibody responses

Cited by 3 publications

References 37 publications

Major histocompatibility complex class II-regulated immunity to murine leukemia virus protects against early T- but not late B-cell lymphomas

Major histocompatibility complex class II-regulated immunity to murine leukemia virus protects against early T- but not late B-cell lymphomas

A host gene regulates the structure of the transmembrane envelope protein of murine leukemia viruses.

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

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