Immunoglobulin Gene Expression in Wasted Mice

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).