作者: G. E. Woloschak , M. Rodriguez , C. J. Krco
DOI: 10.1007/978-1-4684-5344-7_4
关键词:
摘要: 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 this spontaneous autosomal recessive phenotypically manifested in homozygous wst/wst mice at three weeks age as abnormality. animals develop tremor uncoordinated movements followed progressive paralysis. At that time, also manifest lymphoid hypoplasia decreased thymus, lymph node spleen to body weight. Homozygotes (wst/wst) have been show lymphoproliferative responses both Con A LPS with increasing (2). addition, demonstrate increased susceptibility chromosomal injury (1). combined immunologic dysfunction well an propensity for chromosome damage has suggested provides model ataxia telangiectasia (1,3–4).