Advertisement

Immunoglobulin Gene Expression in Wasted Mice

  • G. E. Woloschak
  • M. Rodriguez
  • C. J. Krco
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 216 A)

Abstract

In 1982, Shultz et al. (1) reported the discovery of a new mouse mutation called “wasted” (wst) which is characterized by faulty DNA repair, neurologic abnormalities and immunodeficiency. The disease produced by this spontaneous autosomal recessive mutation (wst) is phenotypically manifested in homozygous wst/wst mice at three weeks of age as a neurologic abnormality. The animals develop tremor and uncoordinated movements which is followed by progressive paralysis. At that time, the animals also manifest lymphoid hypoplasia characterized by decreased thymus, lymph node and spleen to body weight. Homozygotes (wst/wst) have been reported to show decreased lymphoproliferative responses to both Con A and LPS with increasing age (2). In addition, wst/wst mice demonstrate increased susceptibility to chromosomal injury (1). The combined neurologic and immunologic dysfunction as well as an increased propensity for chromosome damage has suggested that the “wasted” mutation provides a model for ataxia telangiectasia (1,3–4).

Keywords

Amyotrophic Lateral Sclerosis Mesenteric Lymph Node Immunologic Abnormality Anterior Horn Cell Human Amyotrophic Lateral Sclerosis 
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. 1.
    Shultz, L.D., Sweet, H.O., Davisson, M.J., Coman, D.R., Nature 297, 402, 1982.PubMedCrossRefGoogle Scholar
  2. 2.
    Goldowitz, D., Shipman, P.W., Porter, J.F. and Schmidt, R.R., J. Immunol. 135, 1806, 1985.PubMedGoogle Scholar
  3. 3.
    Swift, M., in Ataxia-Telangiectasia—A Cellular and Molecular Link Between Cancer, Neuropathology and Immune Deficiency, (Edited by Bridges, B. and Harnden, D.G.), pp. 355–361, 1982.Google Scholar
  4. 4.
    Bridges, B.A., Lenoir, G. and Tomatis, L., Cancer Research 45, 3979, 1979.Google Scholar
  5. 5.
    Kaiserlian, D., Delacroix, D. and Bach, J.R., J. Immunol. 135, 1126, 1985.PubMedGoogle Scholar
  6. 6.
    Woloschak, G.E., Molec. Immunol. 23, 581, 1986.CrossRefGoogle Scholar
  7. 7.
    Woloschak, G.E., Tornasi, T.B. and Liarakos, C.D., Molec. Immunol. 23, 645, 1986.CrossRefGoogle Scholar
  8. 8.
    Woloschak, G.E., Dweald, G., Bahn, R.S., Kyle, P.R., Greipp, P.R. and Ash, R.C., J. Cell. Biochem., 32, 23, 1986.PubMedCrossRefGoogle Scholar
  9. 9.
    Dobner, P.R., Kawasaki, Z.S., Yu, L.-Y. and Bancroft, F.C., Proc. Natl. Acad. Sci. 78, 2230, 1986.CrossRefGoogle Scholar

Copyright information

© Plenum Press, New York 1987

Authors and Affiliations

  • G. E. Woloschak
    • 1
  • M. Rodriguez
    • 1
  • C. J. Krco
    • 1
  1. 1.Departments of Immunology, Biochemistry and Molecular Biology, and Neurology, Mayo Clinic and FoundationRochesterUSA

Personalised recommendations