Virology, genetic and immunology of murine lymphomagenesis

Zijlstra, Maarten; Melief, Cornelis J.M.

doi:10.1016/0304-419x(86)90028-4

Cited by 15 publications

(7 citation statements)

References 392 publications

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“…1). A similar unresponsiveness has been observed in mice congenitally or neonatally infected with other viruses, such as murine leukaemia virus (MuLV; Zijstra & Melief, 1986;Korostoff et al, 1990) or lymphocytic choriomeningitis virus (LCMV; Buchmeier et al, 1980;King et al, 1992). Persistent immune tolerance requires the continuous elimination or inactivation of LDV-specific B cell clones and/or the elimination of LDV-specific CD4 ÷ T-helper cells in the thymus (Nossal, 1989).…”

Section: Discussionsupporting

confidence: 53%

Neonatal Infection of Mice With Lactate Dehydrogenase-elevating Virus Results in Suppression of Humoral Antiviral Immune Response but does not Alter the Course of Viraemia or the Polyclonal Activation of B Cells and Immune Complex Formation

Rowland

Even

Anderson

et al. 1994

Journal of General Virology

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Neonatal infection of FVB mice with lactate dehydrogenase-elevating virus (LDV) prevented the normal formation of anti-LDV antibodies observed in mice infected at 5 days of age or older. Even 22 weeks post-infection, the concentration of circulating anti-LDV antibodies in neonatally infected mice was insignificant. However, the time course and level of persistent viraemia were the same in neonatally infected mice lacking anti-LDV antibodies as in mice infected at 5 or 15 days of age which developed normal antiviral immune responses. The results support the view that LDV replication in mice is unaffected by antiviral immune responses and instead is primarily dependent on the rate of regeneration of LDV-permissive macrophages. This view is further supported by the following findings. Treatment of mice with cyclophosphamide or dexamethasone, which are known to increase plasma LDV levels, increased the proportion of LDV-permissive macrophages in the peritoneum. Injection of mice with interleukin-3, which is known to stimulate macrophage development, increased plasma LDV levels in persistently infected mice 10-to 100-fold. During the first month of age when mice possess a higher proportion of LDV-permissive macrophages than older mice and peritoneal macrophages exhibit self-sustained growth, the persistent plasma LDV titres were also 10-to 100-fold higher than in older mice. The polyclonal activation of B cells induced by LDV that results in a permanent elevation of IgG2a or IgG2b in the circulation, and the formation of 180K to 300K immune complexes containing IgG2a or IgG2b were also the same in neonatally infected mice and mice infected 5 or 15 days after birth. Thus, the polyclonal activation of B cells occurs in the absence of an antiviral humoral immune response and the immune complexes do not contain anti-LDV antibodies. The immune complexes probably consist of autoantibodies formed in the course of the polyclonal activation of B cells and their cellular antigens.

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Section: Discussionsupporting

confidence: 53%

Neonatal Infection of Mice With Lactate Dehydrogenase-elevating Virus Results in Suppression of Humoral Antiviral Immune Response but does not Alter the Course of Viraemia or the Polyclonal Activation of B Cells and Immune Complex Formation

Rowland

Even

Anderson

et al. 1994

Journal of General Virology

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“…For example, trisomy of chromosome 15 was found at high frequency in spontaneous lymphomas as well as in lymphomas induced by carcinogens, X-rays, RadLV or Moloney MuLV in AKR/J mice. 14) In addition, a preferential duplication of chromosome 15 derived from the AKR mouse was demonstrated in T cell lymphomas in (AKR×B6)F 1 mice. 15) Ohno et al demonstrated that mineral oil-or pristane-induced plasmacytomas contain nonrandom chromosomal translocations, t(6;15) or t(12;15), 6,7) and Suematsu et al were able to generate monoclonal transplantable plasmacytomas with the chromosomal translocation t(12;15) in interleukin 6 transgenic mice of BALB/c background, but not in those of C57BL/6 background.…”

Section: Discussionmentioning

confidence: 99%

Strain‐dependency of Chromosomal Abnormalities in Lymphomas Developed in Eμ‐myc Transgenic Mice

Akagi

Yamamura

2001

Japanese Journal of Cancer Research

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“…Thus, it does not contain essential susceptibility genes but influences the rate of progression to overt malignancy. More than one MHC gene is involved in the complex, multifactorial development of malignancies (Oomen et al, 1988;Zijlstra and Melief, 1986). …”

mentioning

confidence: 99%

Influence of the major histocompatibility complex on age at onset of chronic lymphoid leukaemia

et al. 1996

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The major histocompatibility complex is one of the interactive factors in the multifactorial model of carcinogenesis. Its main influence in experimental models is on the age at onset of malignancies. We have previously shown a similar effect of homozygosity for HLA-DR53 in CML. In the present study, we investigated 79 patients with CLL and 329 local controls from Germany. In addition to full serotyping, all patients and I I 6 of controls were also typed by HU-DR6 PCR analysis. The homozygosity rates for DR53 in patients under and over the median age (60 years) were 18.6% and 2.9%, respectively ( p = 0.03). In experimental models, the major histocompatibility complex (MHC) has an interactive influence on the development of spontaneous, virally or chemically-induced malignancies (Lilly et al., 1964; Boyse et al., 1972;Faraldo et al., 1979;Oomen et al., 1988;Vasmel et al., 1988). Particular alleles of this polymorphic system influence the incidence and phenotype, as well as the age at onset of malignancies (Vasmel et al., 1988;Miyazawa et al., 1992). The interaction of the MHC is not exerted on transformation of a neoplastic clone but occurs during the pre-leukaemic stage (Chesebro, 1981;Lonai et al., 1982). Thus, it does not contain essential susceptibility genes but influences the rate of progression to overt malignancy. More than one MHC gene is involved in the complex, multifactorial development of malignancies (Oomen et al., 1988;Zijlstra and Melief, 1986). Eight of theThe findings in animal models stimulated similar studies investigating the role of the human MHC (HLA complex) in malignancies. The initial serological studies uncovered some associations but did not establish a strong and consistent influence of HLA antigens on the development of neoplasms (Tiwari and Terasaki, 1985). The haemopoietic malignancies have been the most extensively studied ones (Seremetis et al., 1985;Bortin et al., 1987;Caruso et al., 1987;Richter et al., 1973;Nunez-Roldan et al., 1982; Kilpatrick et al., 1984;Dyer et al., 1986;Cuttner et al., 1994). In leukaemia and lymphoma also, no consistent HLA association has been shown by serology.With the advent of molecular typing methods, this issue has been revisited. Recent studies have shown stronger allelic associations, although genotypes, age and gender effect have usually been overlooked (Apple et al., 1994;Klitz et al., 1994). The first DNA-based study investigating the role of the HLA complex in the development of leukaemia showed a strong influence of several independent genotypes on the age at onset of chronic myeloid leukaemia (CML), the strongest one being homozygosity for the supertypic specificity HLA-DR53 (Dorak et al., 1994a). A second molecular study confirmed the role of this homozygous genotype in increased susceptibility to childhood acute lymphoblastic leukaemia (ALL) and also showed a gender effect (Dorak et al., 1995).In the present study, the same association and its influence on the age at onset of chronic lymphoid leukaemia (CLL) were investigated by DNA analy...

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Virology, genetic and immunology of murine lymphomagenesis

Cited by 15 publications

References 392 publications

Neonatal Infection of Mice With Lactate Dehydrogenase-elevating Virus Results in Suppression of Humoral Antiviral Immune Response but does not Alter the Course of Viraemia or the Polyclonal Activation of B Cells and Immune Complex Formation

Neonatal Infection of Mice With Lactate Dehydrogenase-elevating Virus Results in Suppression of Humoral Antiviral Immune Response but does not Alter the Course of Viraemia or the Polyclonal Activation of B Cells and Immune Complex Formation

Strain‐dependency of Chromosomal Abnormalities in Lymphomas Developed in Eμ‐myc Transgenic Mice

Influence of the major histocompatibility complex on age at onset of chronic lymphoid leukaemia

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