| First Author | Tamura A | Year | 1996 |
| Journal | Cell Immunol | Volume | 168 |
| Issue | 2 | Pages | 220-8 |
| PubMed ID | 8640868 | Mgi Jnum | J:31852 |
| Mgi Id | MGI:79355 | Doi | 10.1006/cimm.1996.0069 |
| Citation | Tamura A, et al. (1996) Inhibition of apoptosis and augmentation of lymphoproliferation in bcl-2 transgenic Fas/Fas ligand-defective mice. Cell Immunol 168(2):220-8 |
| abstractText | 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. |
