Bhandoola A, Yui K, Siegel R M, Zerva L, Greene M I
Department of Pathology, University of Pennsylvania Medical School, Philadelphia.
Int Rev Immunol. 1994;11(3):231-44. doi: 10.3109/08830189409061729.
Mice homozygous for the gld or lpr mutations develop autoimmunity, and a lymphoproliferative disorder involving accumulation of huge numbers of unusual CD4-CD8-TCR alpha beta lo T cells. Here we review our past work with gld mice, and attempt to explain lymphoproliferation in terms of current models of T cell maturation and self-tolerance induction. The availability of molecular probes to the gene products of lpr and gld should shortly lead to a better understanding of the acquisition of self tolerance during T cell maturation and of autoimmunity.
纯合子gld或lpr突变的小鼠会发生自身免疫，以及一种淋巴细胞增生性疾病，其中涉及大量异常的CD4-CD8-TCRαβ低表达T细胞的积累。在这里，我们回顾了我们过去对gld小鼠的研究工作，并试图根据当前的T细胞成熟和自身耐受诱导模型来解释淋巴细胞增生。不久之后，针对lpr和gld基因产物的分子探针的出现应该会使我们对T细胞成熟过程中自身耐受的获得以及自身免疫有更好的理解。
