| First Author | Reap EA | Year | 1995 |
| Journal | J Immunol | Volume | 155 |
| Issue | 11 | Pages | 5455-62 |
| PubMed ID | 7594564 | Mgi Jnum | J:29877 |
| Mgi Id | MGI:77401 | Doi | 10.4049/jimmunol.155.11.5455 |
| Citation | Reap EA, et al. (1995) bcl-2 transgenic Lpr mice show profound enhancement of lymphadenopathy. J Immunol 155(11):5455-62 |
| abstractText | The lpr gene encodes a defective form of the fas gene that mediates apoptosis, and its expression results in autoantibodies and massive lymphadenopathy. bcl-2, another gene locus that affects programmed cell death, acts to inhibit apoptosis. Since multiple mechanisms controlling programmed cell death may contribute to systemic autoimmunity, the effect of the bcl-2 transgene on the lpr model was examined by crossing bcl-2 transgenic and C57BL/6-lpr mice. Compared with bcl-2-/lpr mice, bcl-2+/lpr showed dramatic increases in lymphadenopathy and T cell accumulation, but not in autoantibodies or B cell numbers. Short term transfer studies demonstrated that double negative T cells normally have a limited lifespan, and their survival is enhanced by the bcl-2 transgene. Thus, defects in separate apoptosis mechanisms may combine to produce enhanced pathologic effects. |
