Yamagiwa S, Kuwano Y, Hasegawa K, Sato K, Ohtsuka K, Iiai T, Tomiyama K, Watanabe H, Sugahara S, Seki S, Asakura H, Abo T
Department of Immunology, Niigata University School of Medicine, Japan.
Eur J Immunol. 1996 Jul;26(7):1409-16. doi: 10.1002/eji.1830260702.
Mice carrying the lpr gene, SCG and MRL-lpr/lpr mice, were used to characterize the phenotype and lpr gene of abnormally proliferating T cells in these mice. A major population which expanded in these mice were T cells expressing intermediate (int) levels of T cell receptor (TCR) (and CD3) and the phenotype of interleukin-2 receptor (IL-2R) beta lo alpha- (possibly abnormal TCRint cells). The levels of TCRhi cells of thymic origin (generated through the mainstream of T cell differentiation in the thymus) profoundly decreased after the onset of disease. However, a small population of normal TCRint cells (i.e. IL-2R beta hi alpha-) were also found to exist in all tested organs. For example, the majority of abnormal IL-2R beta lo TCRint cells were CD4-8- CD2-, while normal IL-2R beta hi TCRint cells were a mixture of single-positive cells (mainly CD8+), CD4-8- cells and CD2+ cells. Moreover, normal TCRint cells preferentially produced normal Fas mRNA and Fas molecules from the lpr gene. This phenomenon explains the leaky appearance of normal Fas mRNA and Fas molecules in mice carrying the lpr gene. It is suggested that a small population of IL-2R beta hi TCRint cells are resistant to the lpr genetic abnormality.
携带lpr基因的小鼠，即SCG和MRL - lpr/lpr小鼠，被用于表征这些小鼠中异常增殖T细胞的表型和lpr基因。在这些小鼠中扩增的主要细胞群是表达中等（int）水平T细胞受体（TCR）（和CD3）以及白细胞介素-2受体（IL-2R）β低α - （可能是异常的TCRint细胞）的T细胞。疾病发作后，胸腺来源的TCRhi细胞（通过胸腺中T细胞分化的主流产生）水平大幅下降。然而，在所有测试器官中也发现存在一小部分正常的TCRint细胞（即IL-2Rβ高α - ）。例如，大多数异常的IL-2Rβ低TCRint细胞是CD4 - 8 - CD2 - ，而正常的IL-2Rβ高TCRint细胞是单阳性细胞（主要是CD8 + ）、CD4 - 8 - 细胞和CD2 + 细胞的混合物。此外，可以正常的TCRint细胞优先从lpr基因产生正常的Fas mRNA和Fas分子。这一现象解释了携带lpr基因的小鼠中正常Fas mRNA和Fas分子的渗漏现象。有人提出，一小部分IL-2Rβ高TCRint细胞对lpr基因异常具有抗性。
