Ecotropic and dualtropic mink cell focus-inducing murine leukemia viruses can induce a wide spectrum of H-2 controlled lymphoma types

Zijlstra, Maarten; Goede, R. E. Y. De; Schoenmakers, H. J.; Radaszkiewicz, Thaddäus; Melief, Cornelis J.M.

doi:10.1016/0042-6822(84)90345-3

Cited by 23 publications

(22 citation statements)

References 40 publications

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“…The strains highly susceptible to T-cell lymphomas (AKR/J, C58/J, and HRS/J hrlhr) had an earlier mean age of onset of lymphomas than strains susceptible to other types of lymphomas. These results are similar to those reported previously for other highly lymphomatous strains, including the AKXD RI strains (34,63). Interestingly, the mean age of onset of lymphomas in HRS/J hrlhr and hrl+ mice was similar (313 + 16 versus 293 ± 18 days, respectively).…”

Section: Resultssupporting

confidence: 91%

Comparative molecular genetic analysis of lymphomas from six inbred mouse strains

Mucenski

Bedigian

Shull

et al. 1988

J Virol

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Section: Resultssupporting

confidence: 91%

Comparative molecular genetic analysis of lymphomas from six inbred mouse strains

Mucenski

Bedigian

Shull

et al. 1988

J Virol

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“…A direct link between MHC type and susceptibility to acute viral illness has not been established before . On the other hand, the association between MHC type and susceptibility to chronic disease induction by RNA tumor viruses, where immune mechanisms are probably responsible for protection, is well established (36)(37)(38)(39)(40)(41)(42). In this case, again, the ability to generate a strong MHC-regulated immune response is associated with resistance to the induction of disease.…”

Section: Discussionmentioning

confidence: 99%

Cooperation between cytotoxic and helper T lymphocytes in protection against lethal Sendai virus infection. Protection by T cells is MHC-restricted and MHC-regulated; a model for MHC-disease associations.

Kast¹,

Bronkhorst²,

Waal³

et al. 1986

The Journal of Experimental Medicine

133

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The in vivo importance of class I MHC regulation of the Tc response to a natural pathogenic agent of high virulence was studied on the basis of our previous demonstration of a major difference in the capacity to generate a Sendai virus-specific Tc response between C57BL/6 (B6, H-2b) mice and H-2Kb mutant B6.C-H-2bm1 (bm 1) mice. These two mouse strains differ from each other only in three amino acids in the crucial H-2Kb restriction element for this response. bm 1 mice, in contrast to B6 mice, are Tc nonresponders against this virus, but show Sendai-specific T cell proliferation, antibody production, and DTH reactions, as well as NK cell activity, equal to those of B6 mice. B6, Sendai Tc-deficient bm 1 and T cell-deficient B6 nu/nu mice differ from each other in susceptibility to lethal pneumonia induced by i.n. inoculation of virulent Sendai virus. The lethal dose (LD50) in B6 mice averaged 152 TCID50, in bm 1 mice, 14 TCID50 and in B6 nu/nu mice 0.5 TCID50. The importance of Tc was also shown by the complete protection of B6 nu/nu mice against infection with a lethal virus dose by i.v. injection of a Sendai virus-specific, IL-2-dependent and H-2Kb-restricted B6 Tc clone. In vivo protection by this Tc clone was H-2Kb-restricted. Apart from Tc, an important role for virus-specific Th cells is evident from the difference in susceptibility between bm 1 and B6 nu/nu mice. This conclusion was supported by the demonstration that the mean survival time of B6 nu/nu and bm 1 nu/nu mice could be significantly prolonged, in an I-Ab-restricted manner, by the injection of in vitro-propagated, Sendai-specific B6 or bm 1 Th clones after a lethal dose of Sendai virus, and by the demonstration that inoculation of these Th clones provided help to virus-specific Tc by means of IL-2 production. Strikingly, Th and Tc cooperate in anti-Sendai virus immunity, since permanent survival of lethally infected nu/nu mice was only achieved by inoculation of a mixture of Tc and Th clones or a mixture of a Tc clone and rIL-2. This study provides a unique model for the study of MHC-disease associations.

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“…This finding is consistent with the hypothesis that viral integration is causally associated with lymphoma induction. Newly acquired clonal proviral integrations have also been observed by many laboratories in which lymphomas that arise in other highly viremic, highly lymphomatous mouse strains are studied (1, 2, 43,44). While somatic integrations of mink cell focus-forming (MCF) proviruses have most often been associated with T-cell lymphomas (4,5,9,23,33), somatic ecotropic proviruses are usually associated with B-cell and myeloid tumors (1, 2, 44).…”

mentioning

confidence: 99%

Identification of a common ecotropic viral integration site, Evi-1, in the DNA of AKXD murine myeloid tumors.

Mucenski¹,

Taylor²,

Hartley³

et al. 1988

Mol. Cell. Biol.

195

128

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AKXD-23 recombinant inbred mice develop myeloid tumors at a high frequency, unlike other AKXD recombinant inbred strains which develop B-cell lymphomas, T-cell lymphomas, or both. AKXD-23 myeloid tumors are monoclonal, and their DNA contains somatically acquired proviruses, suggesting that they are retrovirally induced. We identified a common site of ecotropic proviral integration that is present in the DNA of all AKXD-23 myeloid tumors that were analyzed and in the DNA of all myeloid tumors that occur in AKXD strains othefr than AKXD-23. We designated this locus Evi-l (ecotropic viral integration site 1). Rearrangements in the Evi-l locus were also detected in the DNA of a number of myeloid tumors and myeloid cell lines isolated from strains other than AKXD. In contrast, few Evi-l rearrangements were detected in the DNA of Tor B-cell tumors. Evi-) may thus identify a new proto-oncogene locus that is involved in myeloid disease.Mice from 21 of 23 AKXD recombinant inbred mouse strains derived from AKR/J, a strain with a high incidence of lymphoma, and DBA/2J, a strain with a low incidence of lymphoma, develop hematopoietic neoplasms at a high frequency (27; D. J. Gilbert, unpublished data). However, the average age of onset and the cell type of hematopoietic neoplasms varies from strain to strain, suggesting that in these strains a number of genes that affect susceptibility to lymphoma and disease type have been segregated during inbreeding. Mice from six of the AKXD strains died predominantly of T-cell lymphomas, mice from six strains died predominantly of B-cell lymphomas, and mice from one strain died predominantly of myeloid tumors. Mice from eight strains were equally susceptible to lymphomas of T-or B-cell origin.Most AKXD lymphomas are monoclonal, as evidenced by clonal integrations of somatically acquired proviruses into their DNA (26; D. J. Gilbert, unpublished data). This finding is consistent with the hypothesis that viral integration is causally associated with lymphoma induction. Newly acquired clonal proviral integrations have also been observed by many laboratories in which lymphomas that arise in other highly viremic, highly lymphomatous mouse strains are studied (1, 2,43,44). While somatic integrations of mink cell focus-forming (MCF) proviruses have most often been associated with T-cell lymphomas (4,5,9,23,33), somatic ecotropic proviruses are usually associated with B-cell and myeloid tumors (1, 2, 44). A similar situation exists in AKXD strains (26; D. J. Gilbert, unpublished data).DNAs from 258 AKXD hematopoietic neoplasms were recently characterized to determine whether they contain virally induced rearrangements in seven known or putative proto-oncogene loci found previously to serve as common ). These loci included Myc, Myb, Fis-1, Pim-1, Pvt-J, Mlvi-1, and Mlvi-2. With the exception of Myb, virally induced rearrangements were identified in all loci. Most of these rearrangements were detected in the DNA of T-cell lymphomas; few rearrangements were detected in the DNA of B-cell lymphomas o...

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Ecotropic and dualtropic mink cell focus-inducing murine leukemia viruses can induce a wide spectrum of H-2 controlled lymphoma types

Cited by 23 publications

References 40 publications

Comparative molecular genetic analysis of lymphomas from six inbred mouse strains

Comparative molecular genetic analysis of lymphomas from six inbred mouse strains

Cooperation between cytotoxic and helper T lymphocytes in protection against lethal Sendai virus infection. Protection by T cells is MHC-restricted and MHC-regulated; a model for MHC-disease associations.

Identification of a common ecotropic viral integration site, Evi-1, in the DNA of AKXD murine myeloid tumors.

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