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

M. Prochazka, H. R. Gaskins, L. D. Shultz, E. H. Leiter

Research output: Contribution to journalArticlepeer-review


Homozygosity 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.

Original languageEnglish (US)
Pages (from-to)3290-3294
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Issue number8
StatePublished - 1992
Externally publishedYes


  • severe combined immunodeficiency mutation

ASJC Scopus subject areas

  • General

Fingerprint Dive into the research topics of 'The nonobese diabetic scid mouse: Model for spontaneous thymomagenesis associated with immunodeficiency'. Together they form a unique fingerprint.

Cite this