The nonobese diabetic scid mouse: model for spontaneous thymomagenesis associated with immunodeficiency.

dc.creatorProchazka, M
dc.creatorGaskins, H R
dc.creatorShultz, L D
dc.creatorLeiter, E H
dc.date1992-04-15
dc.date.accessioned2026-08-03T01:32:07Z
dc.descriptionHomozygosity for the severe combined immunodeficiency (scid) mutation results in a block in T- and B-lymphocyte development. An unusually high incidence of spontaneous thymic lymphoma development was observed after transfer of this mutation from the C.B-17 congenic strain background onto the diabetes-susceptible nonobese diabetic (NOD) background. Thymomagenesis in the NOD-scid/scid mouse was associated with expression of an NOD mouse-unique endogenous ecotropic murine leukemia provirus locus (Emv-30, mapped to proximal region of chromosome 11) not expressed in the standard substrain NOD/Lt thymus. All tumors exhibited insertions of ecotropic proviruses, whereas only a subset also exhibited proviral integrations of mink cell focus-forming retrovirus. Neither class of retrovirus was associated with consistent integration into genes previously associated with activation of oncogenesis. We propose that the unusual features of T-cell ontogeny characteristic of the NOD inbred strain synergize with the scid-imparted block in thymocyte development, leading to activation of the NOD-unique Emv-30 to initiate thymomagenesis. IMAGES:
dc.identifierhttps://pmc.ncbi.nlm.nih.gov/articles/PMC48852/
dc.identifierhttps://pubmed.ncbi.nlm.nih.gov/1373493/
dc.identifierhttps://doi.org/10.1073/pnas.89.8.3290
dc.identifier.urihttps://repo.dare.co.zw/handle/123456789/155414
dc.languageen
dc.publisherNational Academy of Sciences
dc.sourceProc Natl Acad Sci U S A
dc.subjectResearch Article
dc.titleThe nonobese diabetic scid mouse: model for spontaneous thymomagenesis associated with immunodeficiency.
dc.typeText

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