Tamura A, Katsumata M, Greene M I, Yui K
Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia 19104, USA.
Cell Immunol. 1996 Mar 15;168(2):220-8. doi: 10.1006/cimm.1996.0069.
Mice defective in Fas (CD95 or APO-1) or its ligand (lpr or gld mice) develop age-dependent lymphadenopathy and systemic autoimmune disease. T cells accumulating in the lymph nodes of these mice express reduced levels of Bcl-2 protein and are susceptible to spontaneous and glucocorticoid-induced apoptosis. We backcrossed bcl-2 transgenic mice to lpr and gld mice to homozygosity to determine the effects of Bcl-2 overexpression. T cells in these mice were resistant to spontaneous and glucocorticoid-induced apoptosis in vitro. Moreover, the accumulation of CD4(-)CD8(-) T cells in the lymph nodes and the spleens was augmented, suggesting that a Bcl-2-dependent mechanism regulating the number of T cells residing in the peripheral lymphoid organs in addition to the Fas-mediated pathway exists.
Fas（CD95或APO-1）或其配体存在缺陷的小鼠（lpr或gld小鼠）会出现年龄依赖性淋巴结病和全身性自身免疫性疾病。在这些小鼠淋巴结中积聚的T细胞表达的Bcl-2蛋白水平降低，并且易发生自发性凋亡以及糖皮质激素诱导的凋亡。我们将bcl-2转基因小鼠与lpr和gld小鼠回交至纯合状态，以确定Bcl-2过表达的影响。这些小鼠的T细胞在体外对自发性凋亡和糖皮质激素诱导的凋亡具有抗性。此外，淋巴结和脾脏中CD4(-)CD8(-) T细胞的积聚增加，这表明除了Fas介导的途径外，还存在一种调节外周淋巴器官中T细胞数量的Bcl-2依赖性机制。
