The scid Mouse Mutant

  • M. Bosma
  • W. Schuler
  • G. Bosma
Part of the Current Topics in Microbiology and Immunology book series (CT MICROBIOLOGY, volume 137)

Abstract

The scid mutation occurred in the C.B-17Icr (C.B-17) inbred strain, an immunoglobulin heavy chain (Igh) congenic partner strain of BALB/cAnlcr (BALB/c) . The C.B-17 strain was derived from the 13th backcross generation of the original C.B stock of M. Potter. C.B-17 mice are not known to differ from BALB/c mice except that a portion of their chromosome 12 comes from the C57BL/Ka strain and includes the C57BL/Ka Igh locus and other closely-linked genes.

Keywords

Scid Mouse Severe Combine Immunodeficiency Severe Combine Immune Deficiency Antigen Receptor Gene Abelson Murine Leukemia 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. Allison JP, Lanier LL (1987) The T cell antigen receptor gamma gene: rearrangement and cell lineages. Immunol. Today 8: 293–296.CrossRefGoogle Scholar
  2. Alt FW, Rosenberg N, Enea V, Siden E, Baltimore D (1982) Multiple immunoglobulin heavy-chain gene transcripts in Abelson murine leukemia virus-transformed lymphoid cell lines. Molec. Cell. Biol. 2: 386–400.PubMedGoogle Scholar
  3. Bancroft GJ, Bosma MJ, Bosma GC, Unanue ER (1986) Regulation of macrophage la expression in mice with severe combined immunodeficiency: induction of la expression by a T cell-independent mechanism. J. Immunol. 137: 4–9.PubMedGoogle Scholar
  4. Bosma GC, Custer RP, Bosma MJ (1983) A severe combined immunodeficiency mutation in the-mouse. Nature 301: 527–530.PubMedCrossRefGoogle Scholar
  5. Bosma GC, Fried M, Custer RP, Carroll A, Gibson D, Bosma MJ (1987) Evidence of functional lymphocytes in some (leaky) scid mice. J. Exp. Med. (in press) .Google Scholar
  6. Custer RP, Bosma GC, Bosma MJ (1985) Severe combined immunodeficiency (SCID) in the mouse: pathology, reconstitution, neoplasms. J. Amer. J. Pathol. 120: 464–477.Google Scholar
  7. Czitrom AA, Edwards S, Phillips RA, Bosma MJ, Marrack P, Kappler JW (1985) The function of antigen-presenting cells in mice with severe combined immunodeficiency. J. Immunol. 134: 2276–2280.PubMedGoogle Scholar
  8. Dorshkind K, Keller GM, Phillips RA, Miller RG, Bosma GC, O’Toole M, Bosma MJ (1984) Functional status of cells from lymphoid and myeloid tissues in mice with severe combined immunodeficiency disease. J. Immunol. 132: 1804–1808.PubMedGoogle Scholar
  9. Dorshkind K, Pollack SB, Bosma MJ, Phillips RA (1985) Natural killer (NK) cells are present in mice with severe combined immunodeficiency (scid) . J. Immunol. 134: 3798–3801.PubMedGoogle Scholar
  10. Epstein R, Davisson M, Lehmann K, Akeson EC, Cohn M (1986) Position of Igl-l, md, and Bst loci on chromosome 16 of the mouse. Immunogenetics 23: 78–83.PubMedCrossRefGoogle Scholar
  11. Grosschedl R, Weaver D, Baltimore D, Constantini F (1984) Introduction of a μ immunoglobulin gene into the mouse germ line: specific expression in lymphoid cells and synthesis of functional antibody. Cell 38: 647–658.PubMedCrossRefGoogle Scholar
  12. Hackett J, Bosma GC, Bosma MJ, Bennett M, Kumar V (1986) Transplantable progenitors of natural killer cells are distinct from those of T and B lymphocytes. Proc. Natl. Acad. Sci. (USA) 83: 3427–3431.CrossRefGoogle Scholar
  13. Kemp DJ, Harris AW, Adams JM (1980) Transcripts of the immunoglobulin Cy gene vary in structure and splicing during lymphoid development. Proc. Natl. Acad. Sci. (USA) 77: 7400–7404.CrossRefGoogle Scholar
  14. Kim MG, Schuler W, Bosma MJ, Marcu KB (1988) Aberrant Igh locus rearrangements in A-MuLV pre-B lines of scid mice: evidence for deregulated D-J recombination. Curr. Top. Microbiol, and Immunol, (in press) .Google Scholar
  15. Lennon GC, Perry RP (1985) Cy-containing transcripts initiate heterogeneously within the IgH enhancer region and contain a novel 5’-nontranslatable exon. Nature 318: 475–478.PubMedCrossRefGoogle Scholar
  16. Rosen FS, Cooper MD, Wedgwood RJ (1984) The primary immunodeficiencies. N. Engl. J. Med. 311: 235–242 and 300–310.PubMedCrossRefGoogle Scholar
  17. Schuler W, Schüler A, Bosma MJ (1987) Evidence for defective rearrangement of TCRγ genes in a mouse mutant (scid) with severe combined immune deficiency. J. Cell. Biochem. suppl. HD p 216 (Abstract) .Google Scholar
  18. Schuler W, Weiler IJr Schuler A, Phillips RA, Rosenberg N, Mak TW, Kearney JFr Perry RP, Bösma MJ (1986) Rearrangement of antigen receptor genes is defective in mice with severe combined immune deficiency. Cell 46: 963–972.PubMedCrossRefGoogle Scholar
  19. Storb U, Pinkert C, Arp B, Engler P, Gollahon K, Manz J, Brady W, Brinster RL (1986) Transgenic mice with μ and κ genes encoding antiphosphorylcholine antibodies. J. Exp. Med. 164: 627–641.PubMedCrossRefGoogle Scholar
  20. Van Ness GG, Weigert M, Coleclough C, Mather EL, Kelley DE, Perry RP (1981) Transcription of the unrearranged mouse Cκ locus. Sequence of the initiation region and comparison of activity with a rearranged Vκ-Cκ gene. Cell 27: 593–602.PubMedCrossRefGoogle Scholar
  21. Yancopoulos G, Alt FW (1985) Developmentally controlled and tissue-specific expression of unrearranged VH gene segments. Cell 40: 271–281.PubMedCrossRefGoogle Scholar

Copyright information

© Springer-Verlag Berlin · Heidelberg 1988

Authors and Affiliations

  • M. Bosma
    • 1
  • W. Schuler
    • 1
  • G. Bosma
    • 1
  1. 1.Institute for Cancer ResearchFox Chase Cancer CenterPhiladelphiaUSA

Personalised recommendations